Spitfire List Web site and blog of anti-fascist researcher and radio personality Dave Emory.

For The Record  

FTR #1127 Bio-Psy-Op Apocalypse Now, Part 3–The Eugenic Virus

WFMU-FM is pod­cast­ing For The Record–You can sub­scribe to the pod­cast HERE.

You can sub­scribe to e‑mail alerts from Spitfirelist.com HERE.

You can sub­scribe to RSS feed from Spitfirelist.com HERE.

You can sub­scribe to the com­ments made on pro­grams and posts–an excel­lent source of infor­ma­tion in, and of, itself, HERE.

Mr. Emory’s entire life’s work is avail­able on a 32GB flash dri­ve, avail­able for a con­tri­bu­tion of $65.00 or more (to KFJC). Click Here to obtain Dav­e’s 40+ years’ work.

Please con­sid­er sup­port­ing THE WORK DAVE EMORY DOES.

FTR #1127 This pro­gram was record­ed in one, 60-minute seg­ment.

NB: This descrip­tion con­tains mate­r­i­al not includ­ed in the orig­i­nal broad­cast.

Intro­duc­tion: This pro­gram exam­ines one of the mul­ti-lay­ered effects of the Covid-19 “bio-psy-op.” We stress that the demar­ca­tion of these lay­ers is for cog­ni­tive purposes–to enhance under­stand­ing. The lay­ers are part of a uni­fied whole.

In this broad­cast, we focus on the eugenic effects of the virus. We have cov­ered eugen­ics in many broad­casts over the decades. A few of those: FTR #‘s 1075, 1029, 908, 909, 32, 1013. FTR #1013 is of par­tic­u­lar impor­tance, as Trump has used the Covid-19 out­break to halt immi­gra­tion into the U.S.

Before delv­ing into the eugen­ics man­i­fes­ta­tions of the Covid-19 out­break, we high­light some of the recent devel­op­ments in the pan­dem­ic:

  1. A recent report, based on ran­dom test­ing, indi­cat­ed that up to one fifth of New York­ers may have been infect­ed by the virus. If accu­rate, this is an impor­tant piece of infor­ma­tion, indi­cat­ing that, from an epi­demi­o­log­i­cal stand­point, the virus did NOT orig­i­nate in Chi­na.
  2. We strong­ly sus­pect that New York was delib­er­ate­ly vec­tored by fas­cist ele­ments asso­ci­at­ed with the Trump admin­is­tra­tion at one lev­el, and the Under­ground Reich at anoth­er. This  method­ol­o­gy would not be unprece­dent­ed“. . . . In the sum­mer of 1965, Spe­cial Oper­a­tions men walked into three New York City sub­way sta­tions and tossed light­bulbs filled with Bacil­lus sub­tilis, a benign bac­te­ria, onto the tracks. The sub­way trains pushed the germs through the entire sys­tem and the­o­ret­i­cal­ly killed over a mil­lion pas­sen­gers. . . .
  3. We note increased fin­ger-point­ing at, scape­goat­ing of, Chi­na for the pan­dem­ic, on the part of Britain, Ger­many and France, in addi­tion to Trump and ele­ments of the intel­li­gence com­mu­ni­ty: ” . . . .Wash­ing­ton is simul­ta­ne­ous­ly spread­ing delib­er­ate rumors that the virus could have orig­i­nat­ed in a Chi­nese lab­o­ra­to­ry. Where­as, sci­en­tists vehe­ment­ly refute the alle­ga­tions, Ger­man For­eign Min­is­ter Heiko Maas declared, he ‘does not want to exclude’ that the WHO will have to deal with these issues. On Mon­day, Chan­cel­lor Angela Merkel called on Bei­jing to show ‘trans­paren­cy’ on the issue. . . . At the same time delib­er­ate rumors are being spread in the Unit­ed States that the Covid-19 virus could have orig­i­nat­ed in a Chi­nese lab­o­ra­to­ry — pos­si­bly in bioweapons lab. The US gov­ern­ment indi­cat­ed that it does not rule out this pos­si­bil­i­ty; US intel­li­gence ser­vices are cur­rent­ly inves­ti­gat­ing the issue. . . Lead­ing British and French politi­cians have expressed sim­i­lar views. British For­eign Min­is­ter Dominic Raab has repeat­ed­ly declared that Chi­na will be held respon­si­ble for the Covid-19 pan­dem­ic. French Pres­i­dent Emmanuel Macron has now joined the cam­paign. Regard­ing the pan­demic’s alleged ori­gin, he declared, ‘there are clear­ly things that have hap­pened’ in Chi­na ‘that we don’t know about.’ . . . . ”
  4. We also note a dis­turb­ing aspect of the symp­toms of a cross-vec­tored, genet­i­cal­ly-engi­neered virus that is the pre­cip­i­tat­ing event for the Nazi takover in the US in Ser­pen­t’s Walk: ” . . . . Pacov‑1 pro­duces only a mild, flu-like infec­tion that dis­ap­pears with­in a day or two. Pub­lic health author­i­ties would over­look it, nev­er con­sid­er it a seri­ous epi­dem­ic, and even if they did they’d have to look care­ful­ly to iso­late it. Once a vic­tim is over the ‘flu,’ Pacov‑1 becomes dor­mant and almost unde­tectable. A month or two lat­er, you send in the sec­ond stage: Pacov‑2 is also a virus, just as con­ta­gious as the first, and just as harm­less by itself. It reacts with Pacov‑1 to pro­duce a pow­er­ful coag­u­lant. . . . you die with­in three min­utes. . . .”
  5. The coag­u­lat­ing pathol­o­gy pro­duced by Pacov‑1 and Pacov‑2 in Ser­pen­t’s Walk is unnerv­ing­ly sim­i­lar to one of the many symp­toms of Covid-19 infec­tion: ” . . . . Doc­tors in hot spots across the globe have begun to report an unex­pect­ed preva­lence of blood clot­ting among COVID cas­es, in what could pose a per­fect storm of poten­tial­ly fatal risk fac­tors. . . . . . . It’s grow­ing so com­mon with severe COVID cas­es, doc­tors are rec­og­niz­ing it as a new pat­tern of clot­ting called COVID-19-asso­ci­at­ed coag­u­lopa­thy, or CAC, which is notably asso­ci­at­ed with high inflam­ma­to­ry mark­ers in the blood, like D‑dimer and fib­rino­gen. . . . ‘In the begin­ning of the out­break, we start­ed only giv­ing them med­i­cine to pre­vent clots. We saw that it was­n’t enough,’ Dr. Cristi­na Abad, an anes­the­si­ol­o­gist at Hos­pi­tal Clínicos San Car­los in Madrid, told ABC News. ‘They start­ed hav­ing pul­monary embolisms, so we start­ed [full] anti­co­ag­u­la­tion on every­one.’ . . .”

Eugen­ics, in its prac­tice, might best be described as a pseu­do-sci­en­tif­ic doc­trine attribut­ing fea­tures of racial, eth­nic and socio-eco­nom­ic prej­u­dice to empir­i­cal sci­en­tif­ic fact. ” . . . Eugen­ics is a set of beliefs and prac­tices that aim to improve the genet­ic qual­i­ty of a human pop­u­la­tion,[4][5] typ­i­cal­ly by exclud­ing peo­ple and groups judged to be infe­ri­or, and pro­mot­ing those judged to be supe­ri­or. . . . Many coun­tries enact­ed[49] var­i­ous eugen­ics poli­cies, includ­ing: genet­ic screen­ings, birth con­trol, pro­mot­ing dif­fer­en­tial birth rates, mar­riage restric­tions, seg­re­ga­tion (both racial seg­re­ga­tion and seques­ter­ing the men­tal­ly ill), com­pul­so­ry ster­il­iza­tionforced abor­tions or forced preg­nan­cies, ulti­mate­ly cul­mi­nat­ing in geno­cide. . . .”

Dis­cus­sion of the eugenic aspects of the Covid-19 phe­nom­e­non include:

  1. De fac­to rationing of health care dur­ing the pan­dem­ic in such a way as to poten­tial­ly lethal­ly dis­crim­i­nate against those with dis­abil­i­ties.
  2. Infec­tion and death rates dis­pro­por­tion­ate­ly high among pop­u­la­tions endur­ing the eco­nom­ic and phys­i­o­log­i­cal afflic­tion deriv­ing from prej­u­dice and social dar­win­is­tic doc­trine: African-Amer­i­cans, peo­ple who work in low-pay­ing jobs that require close human con­tact and liv­ing in con­di­tions that do not per­mit social dis­tanc­ing.
  3. The eco­nom­i­cal­ly degrad­ing effect of GOP fis­cal pol­i­cy with regard to pub­lic trans­porta­tion dur­ing the pan­dem­ic.
  4. New York City has been stig­ma­tized dur­ing the pan­dem­ic, as has New York State.  With large Jew­ish, African-Amer­i­can and Lati­no pop­u­la­tions, a tra­di­tion of lib­er­al pol­i­tics, gen­er­ous munic­i­pal union con­tracts, a free city uni­ver­si­ty pro­gram, New York has long been viewed as “Jew York City” by fas­cist ele­ments. Gov­er­nors, as well as Trump him­self, have pro­posed quar­an­ti­ning New York City and New Jer­sey. This fur­ther under­scores the above spec­u­la­tion con­cern­ing the rate of infec­tion in New York City. ” . . . . As Pres­i­dent Trump put it in his short-lived bid to ‘QUARANTINE’ New York, New Jer­sey and Con­necti­cut, ‘Some peo­ple would like to see New York quar­an­tined because it’s a hot spot’ — the impli­ca­tion being that if New York­ers could only be kept where they are, with check­points and guards if need be, Covid-19 could be stopped from spread­ing else­where in the coun­try. Gov. Ron DeSan­tis of Flori­da set up check­points to stop cars with New York or Louisiana license plates, so that state troop­ers can warn dri­vers to self-quar­an­tine or face 60 days in jail — even as he hes­i­tat­ed to put any social dis­tanc­ing in place or close the beach­es for spring break. Instead of admit­ting the dan­ger of com­mu­ni­ty spread in Flori­da, the gov­er­nor framed the prob­lem as one of out­siders bring­ing germs in. Gov­er­nors in Mary­land and oth­er states warned any­one arriv­ing from the New York City area to iso­late them­selves. On Twit­ter, Covid-19 has tak­en on a new sobri­quet: the ‘Cuo­movirus.’ . . .”

The broad­cast con­cludes with an overview of New York Times head­lines, illus­trat­ing var­i­ous aspects of the socio-eco­nom­ic fall­out of the Covid-19 out­break, vic­tim­iz­ing low­er income peo­ple, reduc­ing income and earn­ing abil­i­ty, edu­ca­tion­al oppor­tu­ni­ty, adverse­ly affect­ing access to food and augur­ing cat­a­stro­phe for Third World pop­u­la­tions:

  1. “Col­leges Run­ning Out of Cash Wor­ry Stu­dents Will Van­ish, Too” by Anemona Har­to­col­lis; The New York Times; 4/16/2020; pp. A1-A-15 [West­ern Edi­tion].
  2.  “Out­break Strains States’ Finances” by Mary Williams Walsh; The New York Times; 4/16/2020; pp. B1-B6 [West­ern Edi­tion].
  3.  ” ‘This Is Going to Kill Small-Town Amer­i­ca’ ” by David Gelles: The New York Times; 4/16/2020; pp. B1-B5 [West­ern Edi­tion].
  4.  The New York Times [West­ern Edi­tion] head­line for 4/16/2020 said it all, as far as the for­tunes of retail out­lets. “Sales at U.S. Stores Hit ‘Cat­a­stroph­ic’ Depths” by Sap­na Mahesh­wari and Ben Cas­sel­man; The New York Times; 4/16/2020.
  5.  “Evi­dence of Virus Effect on Econ­o­my Grows More Omi­nous” [AP]; The New York Times; 4/15/2020.
  6.  “135 Mil­lion Face Star­va­tion. That Could Dou­ble” by Abdi Latif Dahir; The New York Times; 4/23/2020; pp. A1-A6; [West­ern Edi­tion].
  7.  “This Pan­dem­ic Is Bring­ing Anoth­er” by Nicholas Kristof; The New York Times; 4/23/2020; p. A23 [Op-ed–Western Edi­tion].
  8.  “Covid-19 Threat­ens Glob­al Safe­ty Net” Edi­to­r­i­al; The New York Times; 4/23/2020; p. A22 [West­ern Edi­tion].
  9. “How Gov­ern­ment ‘Failed the Elder­ly’ ” Let­ter to the Edi­tor; The New York Times; 4/23/2020; p. A22 [West­ern Edi­tion].
  10.  “A Lim­it on Trump’s Immi­gra­tion Pow­er” by Jen­nifer M. Cha­con and Erwin Cher­merin­sky; The New York Times; 4/23/2020; p. A23 [op-ed–Western Edi­tion].
  11.  ” ‘The Food Sup­ply Chain Is Break­ing.’ Tyson Foods Warns of Meat Short­age as Plants Close Due to Covid-19” by Sanya Man­soor [Time] Yahoo News; 4/26/2020.

As not­ed in the pro­gram, the eugenic aspects of the pan­dem­ic and effects on the eco­nom­i­cal­ly and social­ly dis­ad­van­taged inside and out­side of the U.S. are inex­tri­ca­ble with the weal-con­cen­trat­ing aspects of the pan­dem­ic. This will be the focus of our next pro­gram:

  1. “Banks Steered Rich­est Clients To Fed­er­al Aid” by Emi­ly Flit­ter and Sta­cy Cow­ley; The New York Times; 4/23/2020; pp. A1-A14 [West­ern Edi­tion].
  2. “Mil­lions In Relief For Backer Of Resorts” by Jean­na Smi­alek, Jim Tanker­s­ley and Alan Rappe­port; The New York Times; 4/23/2020; pp. B1-B5 [West­ern Edi­tion].

Herr Schauble?

Crit­i­cal obser­va­tions by Wolf­gang Schauble, the German/EU “Aus­ter­i­ty Czar” who wrought so much suf­fer­ing fol­low­ing the 2008 eco­nom­ic col­lapse has clear­ly enun­ci­at­ed the func­tion­al and philo­soph­i­cal essence of “cor­po­ratist” and eugenic doc­trine. 

This, too, is reflect­ed in the Trumpian “LIBERATE MICHIGAN etc.”

Some back­ground on Schauble’s out­look: ” . . . . Hard­ly a Ger­man gov­ern­ment rep­re­sen­ta­tive is more noto­ri­ous than Wolf­gang Schäu­ble — world­wide. Dur­ing the inter­na­tion­al finan­cial cri­sis, when Schäu­ble was Ger­many’s Min­is­ter of Finance, his EU coun­ter­parts trem­bled: Schäu­ble want­ed to force them to adapt harsh aus­ter­i­ty mea­sures. Because the fore­see­able social con­se­quences would cost lives, Schäuble’s tac­tics seemed to scare Europe with ‘trau­mat­ic effects’ and gave it a les­son in Ger­man eco­nom­ic ethics: Teu­ton­ic bru­tal­i­ty and at all costs. ‘Ter­ri­fy­ing,’ was the assess­ment the US Trea­sury Sec­re­tary made fol­low­ing his con­ver­sa­tion with Schäu­ble. Paris and Madrid were also appre­hen­sive; Athens called Schäu­ble an ‘arson­ist,’ on a ram­page through Europe. Schäu­ble has since climbed high­er on the gov­ern­ment lad­der. Schäu­ble now ranks sec­ond, after the Pres­i­dent, in the Fed­er­al Repub­lic of Ger­many’s pro­to­co­lary sys­tem. . . . .”

After the onset of the Covid-19 pan­dem­ic, he has redou­bled his “Teu­ton­ic bru­tal­i­ty:” ” . . . . In the midst of the Coro­na cri­sis, Schäu­ble ini­ti­at­ed an inter­view, con­sid­ered to be an unof­fi­cial guide­line for the Ger­man state’s life and death deci­sions. Its tenor deserves atten­tion, even beyond Ger­many’s bor­ders.

Should peo­ple have to die, because they are deprived of state resources, essen­tial for the eco­nom­ic cycle, such as cur­rent­ly dur­ing the Coro­na cri­sis? Does the pro­tec­tion of human life have absolute pri­or­i­ty in state pol­i­cy? In the inter­view, Schäu­ble has elab­o­rat­ed in 2020 on what he had already made clear in 2012, dur­ing the inter­na­tion­al finan­cial cri­sis: ‘If I hear that every­thing else must take a back seat to the preser­va­tion of life, I must say that this, in such unequiv­o­cal­ness, is not right.’ Pro­tec­tion of human life does not have an ‘absolute pri­or­i­ty in our Basic Law.’ Death is com­ing soon­er or lat­er any­way. ‘We are all going to die.’ (April 26, 2020)

Schäuble’s state­ments are exem­plary and are of ‘nation­al sig­nif­i­cance’ declared the Ger­man Ethics Coun­cil. The coun­cil is gov­ern­ment financed and pri­or­i­tizes ‘eco­nom­ic rights.’ They should ‘not be uncon­di­tion­al­ly sub­or­di­nat­ed’ to the pro­tec­tion of human life. There is a sort of rival­ry of val­ues. If the val­ue of life would have pri­or­i­ty, ‘free­dom’ would suf­fer, accord­ing to the unan­i­mous judg­ment of the ethics depart­ment of the Ger­man Eco­nom­ic Insti­tute (IW). From the stand­point of Ger­man con­sti­tu­tion­al law, accord­ing to a for­mer judge on the con­sti­tu­tion­al court, ‘the state’s effi­cien­cy’ would encounter its lim­its, if life were giv­en top pri­or­i­ty, where ‘every­thing else must lag arbi­trar­i­ly far behind.’

In fact, the gov­ern­men­t’s oblig­a­tion to the con­sti­tu­tion’s high­est val­ue — the pro­tec­tion of life — must be rel­a­tivized, just as Schäu­ble is doing, con­firm the major­i­ty of Ger­many’s gov­ern­ment lead­ers. Promi­nent voic­es from the par­lia­men­tary oppo­si­tion par­ties are also in agree­ment that the pro­tec­tion of human life, as the pri­ma­ry legit­imized duty of the state is a ‘ques­tion of assess­ment.’ From this the FDP draws the con­clu­sion: ‘there­fore, please reopen the busi­ness­es.’ ‘Enable pro­duc­tion.’ In har­mo­ny with Ger­many’s export econ­o­my lob­by­ists and the Pres­i­dent of the Bun­destag, the chair of the Greens is also one of the rel­a­tiviz­ers. He finds him­self in an alleged ‘dilem­ma,’ when he thinks of the pro­tec­tion of life dur­ing the Coro­na cri­sis, while a fel­low Green munic­i­pal politi­cian speaks in plain oper­a­tional terms; ‘Let me tell you quite blunt­ly: We may be sav­ing peo­ple in Ger­many, who, because of their age or seri­ous pre­vi­ous med­ical con­di­tions, may, be dead any­way in a half a year.’ . . . .”

1a. A recent dis­clo­sure that up to one-fifth of peo­ple in New York City have been infect­ed sug­gests that the virus did not orig­i­nate in Chi­na.

“1 in 5 New York­ers May Have had Covid-19, Anti­body Tests Sug­gest” by J. David Good­man and Michael Roth­feld; The New York Times; 4/23/2020.

One of every five New York City res­i­dents test­ed pos­i­tive for anti­bod­ies to the coro­n­avirus, accord­ing to pre­lim­i­nary results described by Gov. Andrew M. Cuo­mo on Thurs­day that sug­gest­ed that the virus had spread far more wide­ly than known.

If the pat­tern holds, the results from ran­dom test­ing of 3,000 peo­ple raised the tan­ta­liz­ing prospect that many New York­ers — as many as 2.7 mil­lion, the gov­er­nor said — who nev­er knew they had been infect­ed had already encoun­tered the virus, and sur­vived. Mr. Cuo­mo also said that such wide infec­tion might mean that the death rate was far low­er than believed. . . .

1b. We con­clude with dis­cus­sion of the super­vi­sion of Ft. Det­rick per­son­nel by Dr. Kurt Blome, the Deputy Sur­geon Gen­er­al of the Third Reich and anoth­er indi­vid­ual incor­po­rat­ed into the U.S. bio­log­i­cal war­fare estab­lish­ment.

We have dis­cussed Blome in, among oth­er pro­grams, FTR # 1012 and AFA #39.

Both Blome and Traub report­ed direct­ly to Reichs­fuhrer SS Hein­rich Himm­ler dur­ing World War II.

Note the 1966 tests on the New York City sub­way sys­tem.

Lab 257: the Dis­turb­ing Sto­ry of the Government’s Secret Plum Island Germ Lab­o­ra­to­ry; by Michael Christo­pher Car­roll; Copy­right 2004 by Michael Christo­pher Car­roll; Harper­Collins [HC]; p. 14.

. . . . Fort Detrick’s Spe­cial Oper­a­tions Divi­sion ran ‘vul­ner­a­bil­i­ty tests’ in which oper­a­tives walked around Wash­ing­ton, D.C., and San Fran­cis­co with suit­cas­es hold­ing Ser­ra­tia marcescens—a bac­te­ria rec­om­mend­ed to Fort Det­rick by Traub’s nom­i­nal super­vi­sor, Nazi germ czar and Nurem­berg defen­dant Dr. Kurt Blome. Tiny per­fo­ra­tions allowed the germs’ release so they could trace the flow of the germs through air­ports and bus ter­mi­nals. Short­ly there­after, eleven elder­ly men and women checked into hos­pi­tals with nev­er-before-seen Ser­ra­tia marcescens infec­tions. One patient died. Decades lat­er when the germ tests were dis­closed, the Army denied respon­si­bil­i­ty. . . . In the sum­mer of 1965, Spe­cial Oper­a­tions men walked into three New York City sub­way sta­tions and tossed light­bulbs filled Bacil­lus sub­tilis, a benign bac­te­ria, onto the tracks. The sub­way trains pushed the germs through the entire sys­tem and the­o­ret­i­cal­ly killed over a mil­lion pas­sen­gers. . . .

1c. In FTR #1126, we exam­ined the Trump admin­is­tra­tion and GOP’s exploita­tion of the Covid-19 out­break as a cam­paign tac­tic and right-wing hints that the virus escaped from a Chi­nese bio­log­i­cal war­fare lab­o­ra­to­ry.

Now, Ger­many, France and Britain are join­ing with the Trump admin­is­tra­tion and the GOP in hint­ing that the coro­n­avirus escaped from a Chi­nese bio­log­i­cal war­fare lab­o­ra­to­ry.

Amer­i­can media voic­es from (pre­dictably) Fox News to (also pre­dictably) The New York Times are orgias­ti­cal­ly dis­sem­i­nat­ing the fresh fer­til­iz­er, act­ing in con­junc­tion with intel­li­gence offi­cers. 

Note that the linked sto­ry about Fox News describes state­ments by right-wing jour­nal­ists, act­ing in con­cert with ele­ments of the intel­li­gence com­mu­ni­ty, inti­mat­ing that offi­cials of the Demo­c­ra­t­ic Par­ty are in bed with Chi­nese intel­li­gence.

This reeks of McCarthy­ism and may well hand Trump vic­to­ry in the fall and, even­tu­al­ly, lead to war.

In fact, there is a high-secu­ri­ty bio­log­i­cal research facil­i­ty in Wuhan at which Chi­nese sci­en­tists, along with Amer­i­can peers, have been study­ing coronaviruses–a source of inter­mit­tent dis­ease trans­mis­sion in Chi­na. This facil­i­ty involves joint research fund­ed, in part, by the Pen­ta­gon.

Sug­ges­tions that the virus could have orig­i­nat­ed in a Chi­nese bioweapons lab are curi­ous­ly blind to events in the Unit­ed States. In ear­ly August of 2019, short­ly before the record­ed start of the out­break in Wuhan, Chi­na, the U.S. Army Med­ical Research Insti­tute of Infec­tious Dis­eases at that facil­i­ty was closed down by the CDC due to mul­ti­ple safe­ty vio­la­tions. “All research at a Fort Det­rick lab­o­ra­to­ry that han­dles high-lev­el dis­ease-caus­ing mate­r­i­al, such as Ebo­la, is on hold indef­i­nite­ly after the Cen­ters for Dis­ease Con­trol and Pre­ven­tion found the orga­ni­za­tion failed to meet biosafe­ty stan­dards. . . . The CDC sent a cease and desist order in July. After USAMRIID received the order from the CDC, its reg­is­tra­tion with the Fed­er­al Select Agent Pro­gram, which over­sees dis­ease-caus­ing mate­r­i­al use and pos­ses­sion, was sus­pend­ed. That sus­pen­sion effec­tive­ly halt­ed all bio­log­i­cal select agents and tox­in research at USAMRIID . . . .”

As the Ger­man For­eign Pol­i­cy arti­cle notes, the tone of both Amer­i­can and Ger­man rhetoric con­cern­ing Covid-19 is rem­i­nis­cent of the delib­er­ate dis­in­for­ma­tion that led to the Amer­i­can inva­sion of Iraq in 2002.

 . . . . Last week­end, US Pres­i­dent Don­ald Trump warned the Peo­ple’s Repub­lic that it should face con­se­quences if it was “know­ing­ly respon­si­ble” for the spread of the pan­dem­ic. Wash­ing­ton is simul­ta­ne­ous­ly spread­ing delib­er­ate rumors that the virus could have orig­i­nat­ed in a Chi­nese lab­o­ra­to­ry. Where­as, sci­en­tists vehe­ment­ly refute the alle­ga­tions, Ger­man For­eign Min­is­ter Heiko Maas declared, he ‘does not want to exclude’ that the WHO will have to deal with these issues. On Mon­day, Chan­cel­lor Angela Merkel called on Bei­jing to show ‘trans­paren­cy’ on the issue. . . .

 . . . . At the same time delib­er­ate rumors are being spread in the Unit­ed States that the Covid-19 virus could have orig­i­nat­ed in a Chi­nese lab­o­ra­to­ry — pos­si­bly in bioweapons lab. The US gov­ern­ment indi­cat­ed that it does not rule out this pos­si­bil­i­ty; US intel­li­gence ser­vices are cur­rent­ly inves­ti­gat­ing the issue. Par­tic­u­lar­ly giv­en the lie about Iraq’s alleged weapons of mass destruc­tion, such an alle­ga­tion must be per­ceived as a threat to lend legit­i­ma­cy to new aggres­sions. . . .

 . . . . Already last week, Ger­man media organs have increas­ing­ly been call­ing Chi­na the “cul­prit” behind the Covid-19 pan­dem­ic out­break. Under the head­line “what Chi­na already owes us,” Ger­many’s Springer press even called for “repa­ra­tions.” (german-foreign-policy.com reported.[5]) Lead­ing British and French politi­cians have expressed sim­i­lar views. British For­eign Min­is­ter Dominic Raab has repeat­ed­ly declared that Chi­na will be held respon­si­ble for the Covid-19 pan­dem­ic. French Pres­i­dent Emmanuel Macron has now joined the cam­paign. Regard­ing the pan­demic’s alleged ori­gin, he declared, “there are clear­ly things that have hap­pened” in Chi­na “that we don’t know about.”[6] It is not clear how Macron can know some­thing exists that he does not know about. It is how­ev­er clear that he seeks to impli­cate Bei­jing. . . .

 “The Sus­pi­cion Cam­paign;” Ger­man For­eign Pol­i­cy; 4/21/2020.

The Ger­man gov­ern­ment is join­ing the US cam­paign of alle­ga­tions against Chi­na regard­ing the Covid-19 pan­dem­ic out­break. Last week­end, US Pres­i­dent Don­ald Trump warned the Peo­ple’s Repub­lic that it should face con­se­quences if it was “know­ing­ly respon­si­ble” for the spread of the pan­dem­ic. Wash­ing­ton is simul­ta­ne­ous­ly spread­ing delib­er­ate rumors that the virus could have orig­i­nat­ed in a Chi­nese lab­o­ra­to­ry. Where­as, sci­en­tists vehe­ment­ly refute the alle­ga­tions, Ger­man For­eign Min­is­ter Heiko Maas declared, he “does not want to exclude” that the WHO will have to deal with these issues. On Mon­day, Chan­cel­lor Angela Merkel called on Bei­jing to show “trans­paren­cy” on the issue. Senior Ger­man mil­i­tary offi­cials have recent­ly been demand­ing that the EU adopt “a joint polit­i­cal-strate­gic response” to Chi­na’s grow­ing strength, because in the Coro­na cri­sis, Bei­jing is gain­ing con­sid­er­able influ­ence. Accord­ing to a recent poll, more than half of the Ital­ian pop­u­la­tion sees Chi­na as a “friend,” while near­ly half see Ger­many as an “ene­my.”

Delib­er­ate Rumors

The Ger­man gov­ern­ment is join­ing the Trump admin­is­tra­tion’s new cam­paign against Chi­na, albeit atten­u­at­ed. On the week­end, Pres­i­dent Trump claimed that the virus “could have been stopped in Chi­na” and warned that the Peo­ple’s Repub­lic “should face con­se­quences” if it was “know­ing­ly respon­si­ble” for the spread.[1] At the same time delib­er­ate rumors are being spread in the Unit­ed States that the Covid-19 virus could have orig­i­nat­ed in a Chi­nese lab­o­ra­to­ry — pos­si­bly in bioweapons lab. The US gov­ern­ment indi­cat­ed that it does not rule out this pos­si­bil­i­ty; US intel­li­gence ser­vices are cur­rent­ly inves­ti­gat­ing the issue. Par­tic­u­lar­ly giv­en the lie about Iraq’s alleged weapons of mass destruc­tion, such an alle­ga­tion must be per­ceived as a threat to lend legit­i­ma­cy to new aggres­sions. There is no proof that the virus orig­i­nat­ed in a lab­o­ra­to­ry. Sci­en­tif­ic stud­ies clear­ly con­clude that it was trans­mit­ted from wild ani­mals to humans.[2]

Open to Sus­pi­cion

Berlin is open to entire­ly unfound­ed sus­pi­cions. For­eign Min­is­ter Heiko Maas is quot­ed say­ing he “does­n’t want to exclude” that “the WHO will have to deal with these issues.”[3] The Min­is­ter of Devel­op­ment Gerd Müller declared that the Peo­ple’s Repub­lic must dis­play “com­plete open­ness” — “par­tic­u­lar­ly regard­ing the ori­gin of the virus.”[4] Already last week, Ger­man media organs have increas­ing­ly been call­ing Chi­na the “cul­prit” behind the Covid-19 pan­dem­ic out­break. Under the head­line “what Chi­na already owes us,” Ger­many’s Springer press even called for “repa­ra­tions.” (german-foreign-policy.com reported.[5]) Lead­ing British and French politi­cians have expressed sim­i­lar views. British For­eign Min­is­ter Dominic Raab has repeat­ed­ly declared that Chi­na will be held respon­si­ble for the Covid-19 pan­dem­ic. French Pres­i­dent Emmanuel Macron has now joined the cam­paign. Regard­ing the pan­demic’s alleged ori­gin, he declared, “there are clear­ly things that have hap­pened” in Chi­na “that we don’t know about.”[6] It is not clear how Macron can know some­thing exists that he does not know about. It is how­ev­er clear that he seeks to impli­cate Bei­jing.

“A Dev­as­tat­ing Impres­sion”

Insight into the Ger­man-Euro­pean involve­ment in the Trump admin­is­tra­tion’s new cam­paign against Chi­na is pro­vid­ed by Ger­man mil­i­tary offi­cials’ recent state­ments. A new work­ing paper by the Fed­er­al Acad­e­my for Secu­ri­ty Pol­i­cy (BAKS), for exam­ple, exam­ines the Covid-19 pan­demic’s poten­tial glob­al polit­i­cal ram­i­fi­ca­tions. The author, Ret. Brig.Gen. Armin Staigis, BAKS Vice-Pres­i­dent (2013 — 2015) today’s Chair of BAKS “Asso­ci­a­tion of Friends” points out that the USA, “up to now the EU’s most impor­tant part­ner” is “erod­ing in the glob­al con­text.” Chi­na, on the oth­er hand, is emerg­ing more and more “on the world stage.” “With its eco­nom­ic pow­er, it is reach­ing the Euro­pean con­ti­nent and is thus ... also becom­ing a polit­i­cal rival.”[7] The EU should “not become a pawn” in the hands of states like Rus­sia (“revan­chists”), the USA (“off course ego­centrics”) or Chi­na (“hun­gry up-starts”). The EU “still has to for­mu­late a joint polit­i­cal strate­gic answer” par­tic­u­lar­ly to the Peo­ple’s Repub­lic’s grow­ing strength. This is all the more impor­tant in light of the polit­i­cal devel­op­ment in the Coro­na cri­sis: “There is a pub­lic per­cep­tion that Chi­na is pro­vid­ing faster and more help­ful sup­port in Europe than the EU and its mem­ber states among them­selves.” This, how­ev­er, is a “dev­as­tat­ing impres­sion.”

Race between the Global Economic Powers

Late last week, Gen­er­al Staff Offi­cer Col. Matthias Rogg, a mem­ber of the board of the Ger­man Insti­tute for Defense and Strate­gic Stud­ies (GIDS), a Bun­deswehr think tank (found­ed in 2018) made a sim­i­lar obser­va­tion. Rogg assumes that in the course of the Coro­na cri­sis, Chi­na will sig­nif­i­cant­ly enhance its inter­na­tion­al influ­ence. “That per­tains to the eco­nom­ic devel­op­ment in coun­tries, for exam­ple in the Mid­dle East or even in Africa, which are not vis­i­bly affect­ed by the epi­dem­ic, but will sure­ly also be seri­ous­ly affect­ed by Coro­na, either direct­ly or indirectly.”[8] There, the Peo­ple’s Repub­lic of Chi­na will be able to secure new influ­ence “through finan­cial, and mate­r­i­al assis­tance.” It should “not be for­got­ten” that it is com­plete­ly uncer­tain “how the USA will eco­nom­i­cal­ly evolve from this cri­sis.” “That means that in the race between the glob­al eco­nom­ic pow­ers, one can assume that Chi­na ... will have a head start and wind up among the win­ners of the cri­sis.” That is grave — after all, with Chi­na, which, for exam­ple, has “offered imme­di­ate assis­tance” to Italy, we are “de fac­to deal­ing with a coun­try from a rival sys­tem.”

Enemy Number One

A cur­rent sur­vey made in Italy shows the prob­lems Ger­man pow­er strate­gists are con­fronting. The Ital­ian sur­vey sug­gests that the sus­pi­cion cam­paign against Chi­na is also aimed at affect­ing Europe. In mid-March it had indi­cat­ed that around two-thirds of the Ital­ians felt EU mem­ber­ship was dis­ad­van­ta­geous to their coun­try. Only four per­cent felt that the Union was pro­vid­ing suf­fi­cient sup­port to Italy dur­ing the Coro­na crisis.[9] Now, since Chi­na’s most recent Covid-19 assis­tance deliv­ery, 52 per­cent of the Ital­ian pop­u­la­tion see Chi­na as a “friend” of Italy; 32 per­cent con­sid­er Rus­sia, who is also pro­vid­ing assis­tance, a “friend,” and only 17 per­cent place the Unit­ed States in this cat­e­go­ry. Among the coun­tries in the sur­vey con­sid­ered an “ene­my” of Italy, first place, with an impres­sive 45 per­cent, went to Germany.[10]

 [1] Trump dro­ht Chi­na mit “Kon­se­quen­zen”. tagesschau.de 19.04.2020.

[2] Vgl. etwa: Kris­t­ian G. Ander­sen, Andrew Ram­baut, W. Ian Lip­kin, Edward C. Holmes, Robert F. Gar­ry: The prox­i­mal ori­gin of SARS-CoV­‑2. Nature Med­i­cine 26 (2020). S. 450–452.

[3] Nils Met­zger: Neue Argu­mente für Labor-The­o­rie? zdf.de 17.04.2020.

[4] Darum nimmt die Kri­tik an Pekings Umgang mit der Coro­n­avirus-Krise zu. tagesspiegel.de 20.04.2020.

[5] See also Bat­tle of Nar­ra­tives.

[6] Vic­tor Mal­let, Roula Kha­laf: FT Inter­view: Emmanuel Macron says it is time to think the unthink­able. ft.com 16.04.2020.

[7] Armin Staigis: Ern­st­fall Europa — Jet­zt! Bun­de­sakademie für Sicher­heit­spoli­tik: Arbeitspa­pi­er 2/20. Berlin, April 2020.

[8] “Chi­na dürfte am Ende zu den Krisen­gewin­nern gehören”. cicero.de 17.04.2020.

[9] See also Ger­many First (II).

[10] Mas­si­m­il­ia

2a. This post is a pre­view of an upcom­ing show in the “Bio-Psy-Op Apoc­a­lypse Now” series. As Mr. Emory has stressed, the pre­sen­ta­tion of these pro­grams in con­cep­tu­al­ly sep­a­rate pack­ages is for pur­pos­es of cog­ni­tive grasp. The con­sum­mate­ly bril­liant, con­sum­mate­ly evil “bio-psy-op” is an exam­ple of six or sev­en dimen­sion­al chess. It oper­ates on a num­ber of dif­fer­ent, over­lap­ping lev­els simul­ta­ne­ous­ly.

Note that the Nazi takeover in Ser­pen­t’s Walk occurs after the coun­try is attacked with genet­i­cal­ly-engi­neered bio­log­i­cal war­fare weapons. Although the nature of the infec­tion is dif­fer­ent, the over­all par­a­digm is iden­ti­cal. “Pacov” might be under­stood in a con­tem­po­rary con­text as stand­ing for “Pan­dem­ic Coro­n­aVirus.”

In Ser­pen­t’s Walk–which we have dis­cussed for decades–the SS go under­ground (which they did), buy into the opin­ion-form­ing media (which they did) and, infil­trate the mil­i­tary (which they have done), and, after a ter­ror­ist attack by genet­i­cal­ly-engi­neered virus­es dec­i­mates large parts of the Unit­ed States, mar­tial law is declared and the Nazis take over. NB: we do not know if “cross-vec­tor­ing” is occur­ring with the Covid-19 virus, how­ev­er that is some­thing to be con­tem­plat­ed and researched.

 Ser­pen­t’s Walk by “Ran­dolph D. Calver­hall;” Copy­right 1991 [SC]; Nation­al Van­guard Books; 0–937944-05‑X; p. 89.

. . . . “Yes. Well. ‘Pacov’ stands for ‘Pan­dem­ic Com­mu­ni­ca­ble Virus,’ one of the ugli­er results of mil­i­tary exper­i­men­ta­tion with recom­bi­nant DNA. Do you know what that is?” . . .

. . . . “Very well, let me tell you in layman’s terms.” Mul­der extend­ed a hand to shush Wrench, who had start­ed to speak. “Pacov con­sists of two sep­a­rate re-work­ings of two DNA chains of exist­ing virus­es. It’s a pig­gy-back weapon, a two-stage oper­a­tion. You send in the first stage. The vec­tors . . . agents of trans­mis­sion . . . for Pacov‑1 are exten­sive. It trav­els through the air, the water, or direct­ly from per­son-to-per­son and is high­ly con­ta­gious. It spreads for hun­dreds of miles, if con­di­tions are opti­mal.  Pacov‑1 pro­duces only a mild, flu-like infec­tion that dis­ap­pears with­in a day or two. Pub­lic health author­i­ties would over­look it, nev­er con­sid­er it a seri­ous epi­dem­ic, and even if they did they’d have to look care­ful­ly to iso­late it. Once a vic­tim is over the ‘flu,’ Pacov‑1 becomes dor­mant and almost unde­tectable. A month or two lat­er, you send in the sec­ond stage: Pacov‑2 is also a virus, just as con­ta­gious as the first, and just as harm­less by itself. It reacts with Pacov‑1 to pro­duce a pow­er­ful coag­u­lant. . . . you die with­in three min­utes. No warn­ing, no vac­cine, no cure. Those not exposed to both stages remain unharmed. . . . Pacov‑2 goes inert, like Pacov‑1 with­in a week or two. Then you get your victim’s coun­try, all his prop­er­ty, in undam­aged con­di­tion. . . . and a lot of corpses to bury.” . . . .    

2b. We note that, although a “coag­u­lant” is not caus­ing the phe­nom­e­non, blood clots are indeed one of the many symp­toms of the Covid-19: ” . . . . Doc­tors in hot spots across the globe have begun to report an unex­pect­ed preva­lence of blood clot­ting among COVID cas­es, in what could pose a per­fect storm of poten­tial­ly fatal risk fac­tors. . . . . . . It’s grow­ing so com­mon with severe COVID cas­es, doc­tors are rec­og­niz­ing it as a new pat­tern of clot­ting called COVID-19-asso­ci­at­ed coag­u­lopa­thy, or CAC, which is notably asso­ci­at­ed with high inflam­ma­to­ry mark­ers in the blood, like D‑dimer and fib­rino­gen. . . . ‘In the begin­ning of the out­break, we start­ed only giv­ing them med­i­cine to pre­vent clots. We saw that it was­n’t enough,’ Dr. Cristi­na Abad, an anes­the­si­ol­o­gist at Hos­pi­tal Clínicos San Car­los in Madrid, told ABC News. ‘They start­ed hav­ing pul­monary embolisms, so we start­ed [full] anti­co­ag­u­la­tion on every­one.’ . . .”

“Why Are So Many Covid-19 Patients Also See­ing Blood Clots?” by Sasha Pezenik and Dr. L. Ned­da Dast­malchi; Good Morn­ing Amer­i­ca; 4/20/2020.

As the COVID-19 pan­dem­ic rav­ages a world still grap­pling with vast uncer­tain­ty over the virus, a new and unnerv­ing pat­tern has emerged in some patients.

Though nov­el coro­n­avirus symp­toms thus far have pre­sent­ed chiefly with­in the res­pi­ra­to­ry sys­tem, the infec­tion is swift­ly show­ing to be an all-out, sys­tem-wide assault that reach­es far past the lungs. Doc­tors in hot spots across the globe have begun to report an unex­pect­ed preva­lence of blood clot­ting among COVID cas­es, in what could pose a per­fect storm of poten­tial­ly fatal risk fac­tors.

In New Orleans, a man in his 30s was admit­ted to the hos­pi­tal a week into treat­ment for the flu, severe­ly sick. Devel­op­ing short­ness of breath, chest pain and an abnor­mal­ly rapid heart rate — he was test­ed for coro­n­avirus — doc­tors real­ized those symp­toms also are typ­i­cal of a pul­monary embolism: a poten­tial­ly dead­ly blood clot that can move from the legs to the lungs and dam­age the heart.

The man’s blood work already showed heart dam­age, though he had no known under­ly­ing med­ical con­di­tions, no recent trav­el, no recent surg­eries. His chest scans, shown first to ABC News, revealed a mas­sive clot. Termed a “sad­dle embo­lus” because it hooks over branch­es of both pul­monary arter­ies, it was severe­ly stress­ing the right side of the heart, unable to push blood against the clot already in its strained state.

“Thank­ful­ly, we were able to find this and treat this ear­ly, oth­er­wise it prob­a­bly would have killed him,” Dr. Siyab Pan­hwar, a car­dio­vas­cu­lar con­sult for the patient, told ABC News. . . .

. . . It’s grow­ing so com­mon with severe COVID cas­es, doc­tors are rec­og­niz­ing it as a new pat­tern of clot­ting called COVID-19-asso­ci­at­ed coag­u­lopa­thy, or CAC, which is notably asso­ci­at­ed with high inflam­ma­to­ry mark­ers in the blood, like D‑dimer and fib­rino­gen. . . .

. . . . In Spain, among the hard­est-hit nations, clot­ting cas­es have become so preva­lent in nov­el coro­n­avirus patients that doc­tors have begun rou­tine­ly treat­ing indi­vid­u­als with ther­a­peu­tic dos­es of anti­co­ag­u­la­tion med­ica­tion.

“In the begin­ning of the out­break, we start­ed only giv­ing them med­i­cine to pre­vent clots. We saw that it was­n’t enough,” Dr. Cristi­na Abad, an anes­the­si­ol­o­gist at Hos­pi­tal Clínicos San Car­los in Madrid, told ABC News. “They start­ed hav­ing pul­monary embolisms, so we start­ed [full] anti­co­ag­u­la­tion on every­one.” . . .

3. The Bio-Psy-Op is man­i­fest­ing eugen­ics application–a bio-psy-op T4 pro­gram, if you will.

“Peo­ple with Dis­abil­i­ties Are Afraid They Will Be Dis­crim­i­nat­ed Against Because of Coro­n­avirus” by Rick Jer­vais; USA Today; 3/26/2020.

. . . . Peo­ple with dis­abil­i­ties and chron­ic health con­di­tions are some of the most vul­ner­a­ble groups dur­ing the coro­n­avirus cri­sis, though often over­looked in the nation­al debate, accord­ing to advo­cates. The virus has infect­ed more than 69,000 Amer­i­cans and led to near­ly more than 1,000 U.S. deaths, accord­ing to a site run by Johns Hop­kins Uni­ver­si­ty

On Wednes­day, 27 U.S. rep­re­sen­ta­tives and five sen­a­tors sent a let­ter to the Depart­ment of Health and Human Ser­vices, or HHS, and U.S. Attor­ney Gen­er­al William Barr, urg­ing them to issue guid­ance to state agen­cies to pro­tect peo­ple with dis­abil­i­ties from being dis­crim­i­nat­ed against dur­ing the out­break. U.S. Rep. Chris Smith, R‑NJ, led the effort. . . .

. . . . One of the con­cerns is whether peo­ple with dis­abil­i­ties will be side­lined for health­care as med­ical equip­ment such as ven­ti­la­tors and hos­pi­tal beds become increas­ing­ly scarce, said Ari Ne’eman, vis­it­ing schol­ar at the Lurie Insti­tute for Dis­abil­i­ty Pol­i­cy at Bran­deis Uni­ver­si­ty in Mass­a­chu­setts.

 A num­ber of states, includ­ing Utah, Ten­nessee and Alaba­ma, have emer­gency con­tin­gency plans that direct hos­pi­tals not to pro­vide med­ical equip­ment, such as ven­ti­la­tors, to peo­ple with cer­tain intel­lec­tu­al and cog­ni­tive dis­abil­i­ties, should that equip­ment become scarce, he said. . . .

4. The “Use­less Bread Gob­blers” are los­ing out.

“Who Should Be Saved First? Experts Offer Med­ical Guid­ance” by Austin Frakt; The New York Times; 3/24/2020.

How do doc­tors and hos­pi­tals decide who gets poten­tial­ly life­sav­ing treat­ment and who doesn’t?

A lot of thought has been giv­en to just such a predica­ment, well before crit­i­cal short­ages from the coro­n­avirus pan­dem­ic.

“It would be irre­spon­si­ble at this point not to get ready to make trag­ic deci­sions about who lives and who dies,” said Dr. Matthew Wynia, direc­tor of the Cen­ter for Bioethics and Human­i­ties at the Uni­ver­si­ty of Col­orado.

Fac­ing this dilem­ma recent­ly — who gets a ven­ti­la­tor or a hos­pi­tal bed — Ital­ian doc­tors sought eth­i­cal coun­sel and were told to con­sid­er an approach that draws on util­i­tar­i­an prin­ci­ples.

In layman’s terms, a util­i­tar­i­an­ism approach would max­i­mize over­all health by direct­ing care toward those most like­ly to ben­e­fit the most from it. If you had only one ven­ti­la­tor, it would go to some­one more like­ly to sur­vive instead of some­one deemed unlike­ly to do so. . . .

5. It is, on the one hand unsur­pris­ing that African Amer­i­cans are con­tract­ing and dying of coro­n­avirus at a high­er rate and, on the oth­er, com­plete­ly in keep­ing with the Far Right agen­da of Trump, Ban­non et al.

“Ear­ly Data Shows African Amer­i­cans Con­tract­ing and Dying of Coro­n­avirus at an Alarm­ing Rate” by Aki­lah John­son and Talia Buford; ProP­ub­li­ca; 4/3/2020.

The coro­n­avirus entered Mil­wau­kee from a white, afflu­ent sub­urb. Then it took root in the city’s black com­mu­ni­ty and erupt­ed.

As pub­lic health offi­cials watched cas­es rise in March, too many in the com­mu­ni­ty shrugged off warn­ings. Rumors and con­spir­a­cy the­o­ries pro­lif­er­at­ed on social media, push­ing the bogus idea that black peo­ple are some­how immune to the dis­ease. And much of the ini­tial focus was on inter­na­tion­al trav­el, so those who knew no one return­ing from Asia or Europe were quick to dis­miss the risk.

Then, when the shel­ter-in-place order came, there was a nat­ur­al push­back among those who recalled oth­er painful gov­ern­ment restric­tions — includ­ing seg­re­ga­tion and mass incar­cer­a­tion — on where black peo­ple could walk and gath­er.

“We’re like, ‘We have to wake peo­ple up,’” said Mil­wau­kee Health Com­mis­sion­er Jeanette Kowa­lik.

As the dis­ease spread at a high­er rate in the black com­mu­ni­ty, it made an even deep­er cut. Envi­ron­men­tal, eco­nom­ic and polit­i­cal fac­tors have com­pound­ed for gen­er­a­tions, putting black peo­ple at high­er risk of chron­ic con­di­tions that leave lungs weak and immune sys­tems vul­ner­a­ble: asth­ma, heart dis­ease, hyper­ten­sion and dia­betes. In Mil­wau­kee, sim­ply being black means your life expectan­cy is 14 years short­er, on aver­age, than some­one white.

As of Fri­day morn­ing, African Amer­i­cans made up almost half of Mil­wau­kee County’s 945 cas­es and 81% of its 27 deaths in a coun­ty whose pop­u­la­tion is 26% black. Mil­wau­kee is one of the few places in the Unit­ed States that is track­ing the racial break­down of peo­ple who have been infect­ed by the nov­el coro­n­avirus, offer­ing a glimpse at the dis­pro­por­tion­ate destruc­tion it is inflict­ing on black com­mu­ni­ties nation­wide.

In Michi­gan, where the state’s pop­u­la­tion is 14% black, African Amer­i­cans made up 35% of cas­es and 40% of deaths as of Fri­day morn­ing. Detroit, where a major­i­ty of res­i­dents are black, has emerged as a hot spot with a high death toll. As has New Orleans. Louisiana has not pub­lished case break­downs by race, but 40% of the state’s deaths have hap­pened in Orleans Parish, where the major­i­ty of res­i­dents are black.

Illi­nois and North Car­oli­na are two of the few areas pub­lish­ing sta­tis­tics on COVID-19 cas­es by race, and their data shows a dis­pro­por­tion­ate num­ber of African Amer­i­cans were infect­ed.

“It will be unimag­in­able pret­ty soon,” said Dr. Celia J. Maxwell, an infec­tious dis­ease physi­cian and asso­ciate dean at Howard Uni­ver­si­ty Col­lege of Med­i­cine, a school and hos­pi­tal in Wash­ing­ton ded­i­cat­ed to the edu­ca­tion and care of the black com­mu­ni­ty. “And any­thing that comes around is going to be worse in our patients. Peri­od. Many of our patients have so many prob­lems, but this is kind of like the nail in the cof­fin.”

The U.S. Cen­ters for Dis­ease Con­trol and Pre­ven­tion tracks vir­u­lent out­breaks and typ­i­cal­ly releas­es detailed data that includes infor­ma­tion about the age, race and loca­tion of the peo­ple affect­ed. For the coro­n­avirus pan­dem­ic, the CDC has released loca­tion and age data, but it has been silent on race. The CDC did not respond to ProPublica’s request for race data relat­ed to the coro­n­avirus or answer ques­tions about whether they were col­lect­ing it at all.

Experts say that the nation’s unwill­ing­ness to pub­licly track the virus by race could obscure a cru­cial under­ly­ing real­i­ty: It’s quite like­ly that a dis­pro­por­tion­ate num­ber of those who die of coro­n­avirus will be black.

The rea­sons for this are the same rea­sons that African Amer­i­cans have dis­pro­por­tion­ate­ly high rates of mater­nal death, low lev­els of access to med­ical care and high­er rates of asth­ma, said Dr. Cama­ra Jones, a fam­i­ly physi­cian, epi­demi­ol­o­gist and vis­it­ing fel­low at Har­vard Uni­ver­si­ty.

“COVID is just unmask­ing the deep dis­in­vest­ment in our com­mu­ni­ties, the his­tor­i­cal injus­tices and the impact of res­i­den­tial seg­re­ga­tion,” said Jones, who spent 13 years at the CDC, focused on iden­ti­fy­ing, mea­sur­ing and address­ing racial bias with­in the med­ical sys­tem. “This is the time to name racism as the cause of all of those things. The over­rep­re­sen­ta­tion of peo­ple of col­or in pover­ty and white peo­ple in wealth is not just a hap­pen­stance. … It’s because we’re not val­ued.”

Five con­gres­sion­al Democ­rats wrote to Health and Human Ser­vices Sec­re­tary Alex Azar, whose depart­ment encom­pass­es the CDC, last week demand­ing the fed­er­al gov­ern­ment col­lect and release the break­down of coro­n­avirus cas­es by race and eth­nic­i­ty.

With­out demo­graph­ic data, the mem­bers of Con­gress wrote, health offi­cials and law­mak­ers won’t be able to address inequities in health out­comes and test­ing that may emerge: “We urge you not to delay col­lect­ing this vital infor­ma­tion, and to take any addi­tion­al nec­es­sary steps to ensure that all Amer­i­cans have the access they need to COVID-19 test­ing and treat­ment.”

Mil­wau­kee, one of the few places already track­ing coro­n­avirus cas­es and deaths by race, pro­vides an ear­ly indi­ca­tion of what would sur­face nation­al­ly if the fed­er­al gov­ern­ment actu­al­ly did this, or local­ly if oth­er cities and states took its lead.

Mil­wau­kee, both the city and coun­ty, passed res­o­lu­tions last sum­mer that were seen as impor­tant steps in address­ing decades of race-based inequal­i­ty.

“We declared racism as a pub­lic health issue,” said Kowa­lik, the city’s health com­mis­sion­er. “It frames not only how we do our work but how trans­par­ent we are about how things are going. It impacts how we man­age an out­break.”

Mil­wau­kee is try­ing to be pur­pose­ful in how it com­mu­ni­cates infor­ma­tion about the best way to slow the pan­dem­ic. It is address­ing eco­nom­ic and logis­ti­cal road­blocks that stand in the way of safe­ty. And it’s being trans­par­ent about who is infect­ed, who is dying and how the virus spread in the first place.

Kowa­lik described watch­ing the virus spread into the city, with­out enough infor­ma­tion, because of lim­it­ed test­ing, to be able to take ear­ly action to con­tain it.

At the begin­ning of March, Wis­con­sin had one case. State pub­lic health offi­cials still con­sid­ered the risk from the coro­n­avirus “low.” Test­ing cri­te­ria was extreme­ly strict, as it was in many places across the coun­try: You had to have symp­toms and have trav­eled to Chi­na, Iran, South Korea or Italy with­in 14 days or have had con­tact with some­one who had a con­firmed case of COVID-19.

So, she said, she wait­ed, won­der­ing: “When are we going to be able to test for this to see if it is in our com­mu­ni­ty?”

About two weeks lat­er, Mil­wau­kee had its first case.

The city’s patient zero had been in con­tact with a per­son from a neigh­bor­ing, pre­dom­i­nate­ly white and afflu­ent sub­urb who had test­ed pos­i­tive. Giv­en how much com­mut­ing occurs in and out of Mil­wau­kee, with some mak­ing a 180-mile round trip to Chica­go, Kowa­lik said she knew it would only be a mat­ter of time before the virus spread into the city.

A day lat­er came the city’s sec­ond case, some­one who con­tract­ed the virus while in Atlanta. Kowa­lik said she start­ed ques­tion­ing the rigid­ness of the test­ing guide­lines. Why didn’t they include domes­tic trav­el?

By the fourth case, she said, “we deter­mined com­mu­ni­ty spread. … It hap­pened so quick­ly.”

With­in the span of a week, Mil­wau­kee went from hav­ing one case to near­ly 40. Most of the sick peo­ple were mid­dle-aged, African Amer­i­can men. By week two, the city had over 350 cas­es. And now, there are more than 945 cas­es coun­ty­wide, with the bulk in the city of Mil­wau­kee, where the pop­u­la­tion is 39% black. Peo­ple of all ages have con­tract­ed the virus and about half are African Amer­i­can.

The county’s online dash­board of coro­n­avirus cas­es keeps up-to-date infor­ma­tion on the racial break­down of those who have test­ed pos­i­tive. As of Thurs­day morn­ing, 19 peo­ple had died of ill­ness relat­ed to COVID-19 in Mil­wau­kee Coun­ty. All but four were black, accord­ing to the coun­ty med­ical examiner’s office. Records show that at least 11 of the deceased had dia­betes, eight had hyper­ten­sion and 15 had a mix­ture of chron­ic health con­di­tions that includ­ed heart and lung dis­ease.

Because of dis­crim­i­na­tion and gen­er­a­tional income inequal­i­ty, black house­holds in the coun­ty earned only 50% as much as white ones in 2018, accord­ing to cen­sus sta­tis­tics. Black peo­ple are far less like­ly to own homes than white peo­ple in Mil­wau­kee and far more like­ly to rent, putting black renters at the mer­cy of land­lords who can kick them out if they can’t pay dur­ing an eco­nom­ic cri­sis, at the same time as peo­ple are being told to stay home. And when it comes to health insur­ance, black peo­ple are more like­ly to be unin­sured than their white coun­ter­parts.

African Amer­i­cans have grav­i­tat­ed to jobs in sec­tors viewed as reli­able paths to the mid­dle class — health care, trans­porta­tion, gov­ern­ment, food sup­ply — which are now deemed “essen­tial,” ren­der­ing them unable to stay home. In places like New York City, the virus’ epi­cen­ter, black peo­ple are among the only ones still rid­ing the sub­way.

“And let’s be clear, this is not because peo­ple want to live in those con­di­tions,” said Gor­don Fran­cis Good­win, who works for Gov­ern­ment Alliance on Race and Equi­ty, a nation­al racial equi­ty orga­ni­za­tion that worked with Mil­wau­kee on its health and equi­ty frame­work. “This is a mat­ter of tak­ing a look at how our his­to­ry kept peo­ple from actu­al­ly being ful­ly includ­ed.”

Fred Roy­al, head of the Mil­wau­kee branch of the NAACP, knows three peo­ple who have died from the virus, includ­ing 69-year-old Lenard Wells, a for­mer Mil­wau­kee police lieu­tenant and a men­tor to oth­ers in the black com­mu­ni­ty. Royal’s 38-year-old cousin died from the virus last week in Atlanta. His body was returned home Tues­day.

Roy­al is hear­ing that peo­ple aren’t nec­es­sar­i­ly being hos­pi­tal­ized but are being sent home instead and “told to self-med­icate.”

“What is alarm­ing about that,” he said, “is that a num­ber of those indi­vid­u­als were sent home with symp­toms and died before the con­fir­ma­tion of their test came back.”

Health Com­mis­sion­er Kowa­lik said that there have been delays of up to two weeks in get­ting results back from some pri­vate labs, but near­ly all of those who died have done so at hos­pi­tals or while in hos­pice. Still, Kowa­lik said she under­stood why some mem­bers in the black com­mu­ni­ty dis­trust­ed the care they might receive in a hos­pi­tal.

In Jan­u­ary, a 25-year-old day care teacher named Tashon­na Ward died after staff at Froedtert Hos­pi­tal failed to check her vital signs. Fed­er­al offi­cials exam­ined 20 patient records and found sev­en patients, includ­ing Ward, didn’t receive prop­er care. The report didn’t reveal the race of those whose records it exam­ined at the hos­pi­tal, which pre­dom­i­nant­ly serves black patients. Froedtert Hos­pi­tal declined to speak to issues raised in the report, accord­ing to a Feb­ru­ary arti­cle from the Mil­wau­kee Jour­nal Sen­tinel, and it had not sub­mit­ted any cor­rec­tive actions to fed­er­al offi­cials.

“What black folks are accus­tomed to in Mil­wau­kee and any­where in the coun­try, real­ly, is pain not being acknowl­edged and con­stant inequities that hap­pen in health care deliv­ery,” Kowa­lik said.

The health com­mis­sion­er her­self, a black woman who grew up in Mil­wau­kee, said she’s all too famil­iar with the city’s endur­ing strug­gles with seg­re­ga­tion and racism. Her moth­er is black and her father Pol­ish, and she remem­bers the sto­ries they shared about try­ing to buy a house as a young inter­ra­cial cou­ple in Sher­man Park, a neigh­bor­hood once off-lim­its to blacks.

“My father couldn’t get a mort­gage for the house. He had to go to the bank with­out my mom,” Kowa­lik said.

It is the same neigh­bor­hood where fury and frus­tra­tion sparked protests that, at times, roiled into riots in 2016 when a Mil­wau­kee police offi­cer fatal­ly shot Sylville Smith, a 23-year-old black man.

And it is the same neigh­bor­hood that has a con­cen­tra­tion of poor health out­comes when you over­lay a heat map of con­di­tions, be it lead poi­son­ing, infant mor­tal­i­ty — and now, she said, COVID-19.

Know­ing which com­mu­ni­ties are most impact­ed allows pub­lic health offi­cials to tai­lor their mes­sag­ing to over­come the dis­trust of black res­i­dents.

“We’ve been told so much mis­in­for­ma­tion over the years about the con­di­tion of our com­mu­ni­ty,” Roy­al, of the NAACP, said. “I believe a lot of peo­ple don’t trust what the gov­ern­ment says.”

Kowa­lik has met — vir­tu­al­ly — with trust­ed and influ­en­tial com­mu­ni­ty lead­ers to dis­cuss out­reach efforts to ensure every­one is on the same page about the impor­tance of stay­ing home and keep­ing 6 feet away from oth­ers if they must go out.

Police and inspec­tors are respond­ing to com­plaints received about “non­com­pli­ant” busi­ness­es forc­ing staff to come to work or not prac­tic­ing social dis­tanc­ing in the work­place. Vio­la­tors could face fines.

“Who are we get­ting these com­plaints from?” she asked. “Many peo­ple of col­or.”

Res­i­dents have been urged to call 211 if they need help with any­thing from find­ing some­thing to eat or a place to stay. And the state has set up two vol­un­tary iso­la­tion facil­i­ties for peo­ple with COVID-19 symp­toms whose liv­ing sit­u­a­tions are unten­able, includ­ing a Super 8 motel in Mil­wau­kee.

Despite the work being done in Mil­wau­kee, experts like Lin­da Sprague Mar­tinez, a com­mu­ni­ty health researcher at Boston University’s School of Social Work, wor­ry that the gov­ern­ment is not pay­ing close enough atten­tion to race, and as the dis­ease spreads, will do too lit­tle to blunt its toll.

“When COVID-19 pass­es and we see the loss­es … it will be deeply tied to the sto­ry of post-World War II poli­cies that left com­mu­ni­ties mar­gin­al­ized,” Sprague said. “Its impact is going to be tied to our his­to­ry and lega­cy of racial inequities. It’s going to be tied to the fact that we live in two very dif­fer­ent worlds.”

6. The out­break is finan­cial­ly hand­i­cap­ping mass tran­sit, fur­ther strain­ing the mean of low-income peo­ple.

“Covid-19 Push­ing Mass Tran­sit to Brink & Low-Income Rid­ers Will Pay The Price” by Ramya Vijaya; Con­sor­tium News; 4/22/2020.

Low-income Amer­i­cans have borne the brunt of the coro­n­avirus pan­dem­ic. They may also get left behind in the recov­ery.

Steep declines in rid­er­ship dur­ing the cri­sis have pushed pub­lic tran­sit sys­tems across the U.S. into deep finan­cial dis­tress. Though Con­gress includ­ed allo­ca­tions for tran­sit in the CARES Actcities said it won’t be near­ly enough. Even major sys­tems in large metro areas like New York City and Wash­ing­ton, D.C., have seri­ous con­cerns about long-term sur­vival with­out more sus­tained sup­port.

Fail­ure of tran­sit sys­tems would be a dis­as­ter for the large pro­por­tion of low income house­holds that depend on bus­es and trains to get to work and else­where – not only in urban areas, but in rur­al ones too.

I’m cur­rent­ly in the mid­dle of a two-year study of trans­port inequal­i­ty in the U.S. One of my ear­ly find­ings is that about 20 per­cent of the poor­est house­holds don’t own a vehi­cle. That would make them entire­ly reliant on pub­lic trans­porta­tion, com­pared with 6 per­cent for all house­holds. . . .

7. Charles Blow ampli­fies the mes­sage in the Politi­co arti­cle above.

“Social Dis­tanc­ing Is A Priv­i­lege” by Charles Blow; The New York Times; 4/5/2020.

Peo­ple like to say that the coro­n­avirus is no respecter of race, class or coun­try, that the dis­ease Covid-19 is mind­less and will infect any­body it can.

In the­o­ry, that is true. But, in prac­tice, in the real world, this virus behaves like oth­ers, screech­ing like a heat-seek­ing mis­sile toward the most vul­ner­a­ble in soci­ety. And this hap­pens not because it prefers them, but because they are more exposed, more frag­ile and more ill.

What the vul­ner­a­ble por­tion of soci­ety looks like varies from coun­try to coun­try, but in Amer­i­ca, that vul­ner­a­bil­i­ty is high­ly inter­sect­ed with race and pover­ty.

Ear­ly evi­dence from cities and states already shows that black peo­ple are dis­pro­por­tion­ate­ly affect­ed by the virus in dev­as­tat­ing ways. As ProP­ub­li­ca report­ed, in Mil­wau­kee Coun­ty, Wis., as of Fri­day morn­ing, 81 per­cent of the deaths were black peo­ple. Black peo­ple make up only 26 per­cent of that coun­ty.

As for Chica­go, WBEZ report­ed Sun­day that “70 per­cent of Covid-19 deaths are black,” and point­ed out about sur­round­ing Cook Coun­ty, “While black res­i­dents make up only 23 per­cent of the pop­u­la­tion in the coun­ty, they account for 58 per­cent of the Covid-19 deaths.”

The Detroit News report­ed last week, “At least 40 per­cent of those killed by the nov­el coro­n­avirus in Michi­gan so far are black, a per­cent­age that far exceeds the pro­por­tion of African-Amer­i­cans in the Detroit region and state.”

If this pat­tern holds true across oth­er states and cities, this virus could have a cat­a­stroph­ic impact on black peo­ple in this coun­try.

And yet, we are still not see­ing an abun­dance of news cov­er­age or nation­al gov­ern­men­tal response that cen­ter on these racial dis­par­i­ties. Many states haven’t even released race-spe­cif­ic data on cas­es and deaths. The fed­er­al gov­ern­ment hasn’t either.

Part­ly for this rea­son, we are left with decep­tive and dead­ly mis­in­for­ma­tion. The per­cep­tion that this is a jet-set­ters’ dis­ease, or a spring break­ers’ dis­ease, or a “Chi­nese virus” as Pres­i­dent Trump likes to say, must be laid to rest. The idea that this virus is an equal-oppor­tu­ni­ty killer must itself be killed.

And, we must dis­pense with the cal­lous mes­sage that the best defense we have against the dis­ease is some­thing that each of us can con­trol: We can all just stay home and keep social dis­tance.

As a report last month by the Eco­nom­ic Pol­i­cy Insti­tute point­ed out, “less than one in five black work­ers and rough­ly one in six His­pan­ic work­ers are able to work from home.”

As the report point­ed out, “Only 9.2 per­cent of work­ers in the low­est quar­tile of the wage dis­tri­b­u­tion can tele­work, com­pared with 61.5 per­cent of work­ers in the high­est quar­tile.”

If you touch peo­ple for a liv­ing, in elder care or child care, if you cut or fix their hair, if you clean their spaces or cook their food, if you dri­ve their cars or build their hous­es, you can’t do that from home.

Stay­ing at home is a priv­i­lege. Social dis­tanc­ing is a priv­i­lege.

The peo­ple who can’t must make ter­ri­ble choic­es: Stay home and risk star­va­tion or go to work and risk con­ta­gion.

And, this isn’t just hap­pen­ing here, it is hap­pen­ing with poor peo­ple around the world, from New Del­hi to Mex­i­co City.

8a. New York City has long been a focal point of right-wing/­fas­cist hatred. With large non-white pop­u­la­tions, a large Jew­ish pop­u­la­tion, a strong lib­er­al polit­i­cal tra­di­tion and the epi­cen­ter of the finan­cial indus­try (viewed by Nazis and their ilk as “Jew­ish”), New York would be a tar­get for vec­tor­ing by Under­ground Reich ele­ments.

The right has been call­ing the virus as the “Cuo­movirus.”

“Scape­goat­ing New York Means Ignor­ing Its Des­per­ate Need” by Kim Phillips-Fein; The New York Times; 4/5/2020.

The anx­ious notes have been arriv­ing in my inbox from peo­ple all over the coun­try: “Watch­ing reports and want­ed to check in.”

I know why they are con­cerned. New York City has emerged as the epi­cen­ter of the coro­n­avirus pan­dem­ic in the Unit­ed States. For those of us in the city — even if we are stay­ing in our apart­ments almost all day, press­ing ele­va­tor but­tons with our elbows or gloved hands when return­ing from a once-a-week jour­ney to the gro­cery store — we are well aware that we are liv­ing at the heart of the storm.

Almost as alarm­ing as the health data, though, is the sug­ges­tion cir­cu­lat­ing in some polit­i­cal cor­ners that New York and New York­ers are to blame for spread­ing for the coro­n­avirus, as though the city helped to cre­ate a health threat now endan­ger­ing the good peo­ple of the South and Mid­west. Once it was the “Chi­nese virus”; now it also belongs to New York.

As Pres­i­dent Trump put it in his short-lived bid to “QUARANTINE” New York, New Jer­sey and Con­necti­cut, “Some peo­ple would like to see New York quar­an­tined because it’s a hot spot” — the impli­ca­tion being that if New York­ers could only be kept where they are, with check­points and guards if need be, Covid-19 could be stopped from spread­ing else­where in the coun­try.

Gov. Ron DeSan­tis of Flori­da set up check­points to stop cars with New York or Louisiana license plates, so that state troop­ers can warn dri­vers to self-quar­an­tine or face 60 days in jail — even as he hes­i­tat­ed to put any social dis­tanc­ing in place or close the beach­es for spring break. Instead of admit­ting the dan­ger of com­mu­ni­ty spread in Flori­da, the gov­er­nor framed the prob­lem as one of out­siders bring­ing germs in. Gov­er­nors in Mary­land and oth­er states warned any­one arriv­ing from the New York City area to iso­late them­selves.

On Twit­ter, Covid-19 has tak­en on a new sobri­quet: the “Cuo­movirus.”

There’s a long his­to­ry of scape­goat­ing New York City for prob­lems that have their roots far beyond the Hud­son. In the 1970s, the Ford admin­is­tra­tion blamed New York’s lib­er­al pol­i­tics, gen­er­ous social safe­ty net and strong pub­lic sec­tor unions for the fis­cal cri­sis that almost brought the city to bank­rupt­cy — even though that cri­sis arose when the coun­try as a whole was mired in reces­sion, at a moment when fed­er­al poli­cies encour­aged sub­ur­ban flight and the depar­ture of fac­to­ries from cities like New York.

Despite the nation­al con­text for the city’s dif­fi­cul­ties, Pres­i­dent Ger­ald Ford warned that there could be no fed­er­al aid for the country’s largest metrop­o­lis because it had brought its prob­lems on itself. As his press sec­re­tary Ron Nessen put it: “This is not a nat­ur­al dis­as­ter or an act of God. It is a self-inflict­ed act by the peo­ple who have been run­ning New York for a long time.”

Under­ly­ing Ford’s puni­tive atti­tude was a deep­er con­ser­v­a­tive cri­tique of the city. Its his­to­ry of left­ist pol­i­tics, its tuition-free city uni­ver­si­ty and its net­work of pub­lic hos­pi­tals (sev­er­al of which were closed in the fis­cal cri­sis) all made New York sus­pect, as did its rep­u­ta­tion as a cen­ter for the gay rights move­ment and fem­i­nism.

The vision of New York as moral­ly sus­pect, a city of sex­u­al promis­cu­ity and lib­er­tine mores, also helped shape the fed­er­al response to the AIDS epi­dem­ic of the 1980s. The Rea­gan admin­is­tra­tion failed so dis­mal­ly in address­ing the health cri­sis, not even men­tion­ing it pub­licly for years after it had emerged, as it raged in part because AIDS was viewed as a dis­ease of the cities, espe­cial­ly of gay men and IV drug users, not as a prob­lem of the heart­land.

But while some aspects of New York’s sit­u­a­tion in the 1970s and beyond were unique, the larg­er prob­lems the city faced were those con­fronting the entire coun­try. And the AIDS epi­dem­ic, too, spread through­out the nation. Blam­ing New York was a way to let the fed­er­al gov­ern­ment off the hook.

Today, the scape­goat­ing of the city could have con­se­quences even more pro­found than dur­ing the 1970s. It could mean the city not get­ting the fed­er­al mon­ey it needs or a suf­fi­cient sup­ply of ven­ti­la­tors and masks and enough sup­port for health care work­ers.

What is more, the sug­ges­tion that New York is unique­ly sus­cep­ti­ble can sup­port the dan­ger­ous illu­sion that allowed the coro­n­avirus to gain trac­tion here in the first place: that we are able to cor­don our­selves off from one anoth­er, that one region of the coun­try — or the world — can be sep­a­rat­ed from the rest. Act­ing on this fan­ta­sy would be the real dan­ger to states like Flori­da, Ver­mont and Ten­nessee.

At the same time, paint­ing a pic­ture of the entire city as equal­ly at risk may make it hard­er to address the like­li­hood that the coro­n­avirus will prob­a­bly have the most dev­as­tat­ing impact on work­ing-class and poor peo­ple — who are less like­ly to have good access to health care, whose under­ly­ing health may be worse to begin with and for whom the eco­nom­ic penal­ties of social dis­tanc­ing are more pro­found.

The dense urban spaces of New York City are emp­ty now — the libraries and pub­lic schools closed, the play­grounds and streets notably qui­et. But the social sol­i­dar­i­ty that they nur­ture still has the capac­i­ty to offer lessons that might help the rest of the coun­try.

I’ve seen this even in my own apart­ment build­ing, where peo­ple have mobi­lized in sup­port of the most at-risk res­i­dents — all from a dis­tance of six feet. High school stu­dents are offer­ing vir­tu­al tutor­ing to home­bound ele­men­tary school kids, younger ten­ants are pick­ing up gro­ceries for elder­ly peo­ple for whom a trip to the store might be more dan­ger­ous, the most orga­nized among us are keep­ing phone lists so that ten­ants can call one anoth­er if any of us get sick and need help.

And as is hap­pen­ing in places around the world, every night at 7 peo­ple come to the win­dows and the bal­conies of my apart­ment com­plex to cheer for the hero­ism and ded­i­ca­tion of the city’s health care work­ers — the E.M.T.s, ambu­lance dri­vers, physi­cian assis­tants, jan­i­tors, cooks, order­lies, doc­tors and nurs­es. As we chant and clap, we can see one anoth­er from the win­dows and across the court­yard, and even in this moment of dev­as­ta­tion, the col­lec­tive life of our city offers sus­te­nance and hope.

8b. Crit­i­cal obser­va­tions by Wolf­gang Schauble, the German/EU “Aus­ter­i­ty Czar” who wrought so much suf­fer­ing fol­low­ing the 2008 eco­nom­ic col­lapse has clear­ly enun­ci­at­ed the func­tion­al and philo­soph­i­cal essence of “cor­po­ratist” and eugenic doc­trine. 

This, too, is reflect­ed in the Trumpian “LIBERATE MICHIGAN etc.”

“Ger­many Threat­ens” by Rudi­ger Minow; Ger­man For­eign Pol­i­cy; 5/01/2020.

Hard­ly a Ger­man gov­ern­ment rep­re­sen­ta­tive is more noto­ri­ous than Wolf­gang Schäu­ble — world­wide. Dur­ing the inter­na­tion­al finan­cial cri­sis, when Schäu­ble was Ger­many’s Min­is­ter of Finance, his EU coun­ter­parts trem­bled: Schäu­ble want­ed to force them to adapt harsh aus­ter­i­ty mea­sures. Because the fore­see­able social con­se­quences would cost lives, Schäuble’s tac­tics seemed to scare Europe with “trau­mat­ic effects” and gave it a les­son in Ger­man eco­nom­ic ethics: Teu­ton­ic bru­tal­i­ty and at all costs. “Ter­ri­fy­ing,” was the assess­ment the US Trea­sury Sec­re­tary made fol­low­ing his con­ver­sa­tion with Schäu­ble. Paris and Madrid were also appre­hen­sive; Athens called Schäu­ble an “arson­ist,” on a ram­page through Europe. Schäu­ble has since climbed high­er on the gov­ern­ment lad­der. Schäu­ble now ranks sec­ond, after the Pres­i­dent, in the Fed­er­al Repub­lic of Ger­many’s pro­to­co­lary sys­tem. What­ev­er he says car­ries weight. And he uses this posi­tion. In the midst of the Coro­na cri­sis, Schäu­ble ini­ti­at­ed an inter­view, con­sid­ered to be an unof­fi­cial guide­line for the Ger­man state’s life and death deci­sions. Its tenor deserves atten­tion, even beyond Ger­many’s bor­ders.

Death Is Com­ing Any­way

Should peo­ple have to die, because they are deprived of state resources, essen­tial for the eco­nom­ic cycle, such as cur­rent­ly dur­ing the Coro­na cri­sis? Does the pro­tec­tion of human life have absolute pri­or­i­ty in state pol­i­cy? In the inter­view, Schäu­ble has elab­o­rat­ed in 2020 on what he had already made clear in 2012, dur­ing the inter­na­tion­al finan­cial cri­sis: “If I hear that every­thing else must take a back seat to the preser­va­tion of life, I must say that this, in such unequiv­o­cal­ness, is not right.” Pro­tec­tion of human life does not have an “absolute pri­or­i­ty in our Basic Law.” Death is com­ing soon­er or lat­er any­way. “We are all going to die.” (April 26, 2020)

Rival­ry of Val­ues

Schäuble’s state­ments are exem­plary and are of “nation­al sig­nif­i­cance” declared the Ger­man Ethics Coun­cil. The coun­cil is gov­ern­ment financed and pri­or­i­tizes “eco­nom­ic rights.” They should “not be uncon­di­tion­al­ly sub­or­di­nat­ed” to the pro­tec­tion of human life. There is a sort of rival­ry of val­ues. If the val­ue of life would have pri­or­i­ty, “free­dom” would suf­fer, accord­ing to the unan­i­mous judg­ment of the ethics depart­ment of the Ger­man Eco­nom­ic Insti­tute (IW). From the stand­point of Ger­man con­sti­tu­tion­al law, accord­ing to a for­mer judge on the con­sti­tu­tion­al court, “the state’s effi­cien­cy” would encounter its lim­its, if life were giv­en top pri­or­i­ty, where “every­thing else must lag arbi­trar­i­ly far behind.”

Enable Pro­duc­tion

In fact, the gov­ern­men­t’s oblig­a­tion to the con­sti­tu­tion’s high­est val­ue — the pro­tec­tion of life — must be rel­a­tivized, just as Schäu­ble is doing, con­firm the major­i­ty of Ger­many’s gov­ern­ment lead­ers. Promi­nent voic­es from the par­lia­men­tary oppo­si­tion par­ties are also in agree­ment that the pro­tec­tion of human life, as the pri­ma­ry legit­imized duty of the state is a “ques­tion of assess­ment.” From this the FDP draws the con­clu­sion: “there­fore, please reopen the busi­ness­es.” “Enable pro­duc­tion.” In har­mo­ny with Ger­many’s export econ­o­my lob­by­ists and the Pres­i­dent of the Bun­destag, the chair of the Greens is also one of the rel­a­tiviz­ers. He finds him­self in an alleged “dilem­ma,” when he thinks of the pro­tec­tion of life dur­ing the Coro­na cri­sis, while a fel­low Green munic­i­pal politi­cian speaks in plain oper­a­tional terms; “Let me tell you quite blunt­ly: We may be sav­ing peo­ple in Ger­many, who, because of their age or seri­ous pre­vi­ous med­ical con­di­tions, may, be dead any­way in a half a year.”

Neglect

Delib­er­ate­ly blunt or ratio­nal­iz­ing inhib­it­ed, deci­sive group­ings with­in Ger­man polit­i­cal and eco­nom­ic pol­i­cy are dis­play­ing clear signs of an eth­i­cal dete­ri­o­ra­tion, where­in the preser­va­tion of eco­nom­ic activ­i­ty is being coun­ter­poised to the preser­va­tion of human life — offen­sive­ly, by seek­ing to depict life as a rival­ing com­mod­i­ty of exis­tence. How­ev­er, prac­ti­cal eco­nom­ic activ­i­ty is no rival to main­tain­ing human life, it trans­forms nature into the prac­ti­cal mate­r­i­al that sus­tains and sat­is­fies life — as long as eco­nom­ic activ­i­ty sup­ports life. How­ev­er, a “dilem­ma” aris­es, when con­crete indi­vid­ual lives must be sac­ri­ficed, because the prac­ti­cal resources of eco­nom­ic activ­i­ty are unavail­able, although the state’s pri­ma­cy for mak­ing, first and fore­most, pro­vi­sions for human life was rea­son­able but neglect­ed. The greater the neglect, the greater are the “ques­tions of assess­ment.”

Escapism

In the cur­rent cri­sis, it is obvi­ous that the prac­ti­cal resources that eco­nom­ic activ­i­ty could have pro­duced for the preser­va­tion of human life, were not or insuf­fi­cient­ly avail­able before death could no longer be avoid­ed. By not pro­vid­ing even the sim­plest means of pro­tec­tion, the offi­cials have shift­ed respon­si­bil­i­ty for life and death “ques­tions of assess­ment” to the hos­pi­tals. This escapism has cost addi­tion­al lives or over­whelmed the lives of many nurs­es and doc­tors.

Bar­bar­ians

Pro­tec­tive means that are now being sup­plied are sub­ject­ed to usu­ri­ous trade; sur­vival machines for inten­sive-care med­i­cine are incit­ing stock mar­ket spec­u­la­tors, bet­ting on com­pa­ny shares of the man­u­fac­tur­ers, increas­ing their wealth. The poor are dying in rest homes and the sub­urbs. As long as the state allows this sit­u­a­tion to con­tin­ue, the preser­va­tion of human life and preser­va­tion of the eco­nom­ic activ­i­ty are indeed in oppo­si­tion to one anoth­er — how­ev­er not as the advo­cates of val­ue rival­ry are intend­ing. A state that relin­quish­es the preser­va­tion of human life, to that of eco­nom­ic free­dom has either giv­en up its exis­tence or become bar­bar­ian.

Fail­ure

It is not sole­ly a Ger­man pecu­liar­i­ty to not draw bound­aries between civ­i­liza­tion and biol­o­gy in the event of state fail­ure. The ide­ol­o­gy of fail­ure adores the dull stench of preda­tor dens, where the stronger ani­mals feed on the weak­er. There, archa­ic instinct makes the preser­va­tion of life super­flu­ous. The preda­tor archa­ic and its eco­nom­ic ide­al — social Dar­win­ism — deter­mine phas­es of Ger­man his­to­ry, where­in the state can no longer con­trol its eco­nom­ic poten­cy; it must be cat­a­pult­ed beyond its bor­ders or col­lapse. Then it will be doubt­ful, whether every­thing else will recede, if the preser­va­tion of life pro­hibits every­thing else, name­ly death. Then a threat can be heard from Ger­many.

Upheaval

How­ev­er, if with death, the high­est oblig­a­tion for the state, the pro­tec­tion of human life, falls, then the state’s right to the monop­oly on the use of force to pro­tect human life against any oth­er claim, falls as well. If the monop­oly on the use of force falls, the state falls into its con­di­tion that rel­a­tivized human life and forces to ele­vate human life again to its per­ma­nent right.

9. “Col­leges Run­ning Out of Cash Wor­ry Stu­dents Will Van­ish, Too” by Anemona Har­to­col­lis; The New York Times; 4/16/2020; pp. A1-A-15 [West­ern Edi­tion].

10. “Out­break Strains States’ Finances” by Mary Williams Walsh; The New York Times; 4/16/2020; pp. B1-B6 [West­ern Edi­tion].

11. ” ‘This Is Going to Kill Small-Town Amer­i­ca’ ” by David Gelles: The New York Times; 4/16/2020; pp. B1-B5 [West­ern Edi­tion].

12. The New York Times [West­ern Edi­tion] head­line for 4/16/2020 said it all, as far as the for­tunes of retail out­lets.

“Sales at U.S. Stores Hit ‘Cat­a­stroph­ic’ Depths” by Sap­na Mahesh­wari and Ben Cas­sel­man; The New York Times; 4/16/2020.

. . . . Total sales, which include retail pur­chas­es in stores and online as well as mon­ey spent at bars and restau­rants, fell 8.7 per­cent from the pre­vi­ous month, the Com­merce Depart­ment said Wednes­day. The decline was by far the largest in the near­ly three decades the gov­ern­ment has tracked the data.

Even that bleak fig­ure does­n’t cap­ture the full impact of the sud­den eco­nom­ic freeze on the retail indus­try. Most states did­n’t shut down nonessen­tial busi­ness­es until late March or ear­ly April, mean­ing data for the cur­rent month could be worse still. . . .

13.  “Evi­dence of Virus Effect on Econ­o­my Grows More Omi­nous” [AP]; The New York Times; 4/15/2020.

14. “135 Mil­lion Face Star­va­tion. That Could Dou­ble” by Abdi Latif Dahir; The New York Times; 4/23/2020; pp. A1-A6; [West­ern Edi­tion].

15. “This Pan­dem­ic Is Bring­ing Anoth­er” by Nicholas Kristof; The New York Times; 4/23/2020; p. A23 [Op-ed–Western Edi­tion].

16. “Covid-19 Threat­ens Glob­al Safe­ty Net” Edi­to­r­i­al; The New York Times; 4/23/2020; p. A22 [West­ern Edi­tion].

17. “How Gov­ern­ment ‘Failed the Elder­ly’ ” Let­ter to the Edi­tor; The New York Times; 4/23/2020; p. A22 [West­ern Edi­tion].

Re “Death Toll Spikes at Nurs­ing Homes as Defens­es Crack’ (front page, April 18).

18a. “A Lim­it on Trump’s Immi­gra­tion Pow­er” by Jen­nifer M. Cha­con and Erwin Cher­merin­sky; The New York Times; 4/23/2020; p. A23 [op-ed–Western Edi­tion].

18b. ” ‘The Food Sup­ply Chain Is Break­ing.’ Tyson Foods Warns of Meat Short­age as Plants Close Due to Covid-19” by Sanya Man­soor [Time] Yahoo News; 4/26/2020.

Tyson Foods, one of the U.S.’s biggest meat proces­sors, didn’t mince words in a full page New York Times spread that ran Sun­day, in which they warned, “the food sup­ply chain is break­ing.”

“As pork, beef and chick­en plants are being forced to close, even for short peri­ods of time, mil­lions of pounds of meat will dis­ap­pear from the sup­ply chain,” John Tyson, Chair­man of the Board of Tyson Foods, wrote in a let­ter pub­lished as an adver­tise­ment. “As a result, there will be lim­it­ed sup­ply of our prod­ucts avail­able in gro­cery stores until we are able to reopen our facil­i­ties that are cur­rent­ly closed.” . . .

19. “Banks Steered Rich­est Clients To Fed­er­al Aid” by Emi­ly Flit­ter and Sta­cy Cow­ley; The New York Times; 4/23/2020; pp. A1-A14 [West­ern Edi­tion].

20. “Mil­lions In Relief For Backer Of Resorts” by Jean­na Smi­alek, Jim Tanker­s­ley and Alan Rappe­port; The New York Times; 4/23/2020; pp. B1-B5 [West­ern Edi­tion].

Discussion

8 comments for “FTR #1127 Bio-Psy-Op Apocalypse Now, Part 3–The Eugenic Virus”

  1. Excel­lent Pro­gram.

    Your arti­cles hit the bullseye.....You are good at that Dave,

    It is very unfor­tu­nate that most peo­ple do not know the true ene­my and blame the wrong par­ties as the pub­lic works against every­thing.

    I sup­pose that is why the Bad Guys are win­ning.

    The world cul­tures are con­trolled by the ene­my and peo­ple are brain­washed and run­ning scared.

    Posted by ed | April 28, 2020, 7:14 pm
  2. Here’s a pair of arti­cles that poten­tial­ly relate to the intrigu­ing pos­si­bil­i­ty that the Trump admin­is­tra­tion could be inten­tion­al­ly try­ing to encour­age the spread of the virus for the pur­pose of obscur­ing phy­lo­ge­net­ic traces of ear­li­er out­breaks of the virus in the US that would under­mine the nar­ra­tive of how the virus emerged in Chi­na and only lat­er infect­ed the US. The first excerpt is about Pres­i­dent Trump’s sur­prise announce­ment that he’ll be giv­ing the West Point com­mence­ment speech in June, which hap­pens to be the per­fect move if encour­ag­ing the spread of new­er viral strains to obscure old­er yet-to-be-offi­cial­ly-dis­cov­ered viral strains was goal.

    The sec­ond arti­cle about new research out of Chi­na that found for the first time a dif­fer­ence in the lev­el of infec­tiv­i­ty between dif­fer­ent strains of the virus. A 270-fold dif­fer­ence in viral lev­els between the weak­est and strongest test­ed strains. And it appears that Europe was pri­mar­i­ly hit by the more vir­u­lent strain which lat­er trav­eled from Europe to New York City. The out­break on US West Coast, on the oth­er hand, was pri­mar­i­ly of the weak­er strain. This find­ing could account in part for the dif­fer­ences in the sever­i­ty of the out­break between the US East Coast and West Coast. And, of course, the find­ing also sug­gest that any West Point cadets that get infect­ed after trav­el­ing to New York for the cer­e­mo­ny in June are going to infect­ed with the more vir­u­lent strains before return­ing home to spread it around:

    First, recall the sto­ry about research done by a team at Cam­bridge Uni­ver­si­ty that used phy­lo­ge­net­ic analy­sis — con­struct­ing fam­i­ly trees of the virus based on com­par­isons of their genom­ic sequences and then mak­ing infer­ences about the tim­ing of the geo­graph­i­cal spread of the virus — found three dis­tinct strains of the virus: Type A, Type B, and Type C. Basi­cal­ly, they looked at all of the viral strains avail­able in the GISAID data­base of viral sequences tak­en from COVID-19 patients, looked at the muta­tions in the sequence, and log­i­cal­ly con­struct­ed fam­i­ly trees of the virus based on those muta­tions using the sim­ple log­ic that if virus a has muta­tions 1,2,3, and 4, it must have emerged from a virus that already had muta­tions 1, 2, and 3 (where the ‘orig­i­nal’ virus did­n’t have any of those muta­tions). Using that sim­ple approach they can infer how the virus evolved and spread around the world.

    And while most of the muta­tions in the virus’s genet­ic sequences don’t actu­al­ly change the amino acid com­po­si­tion of the viral pro­teins (some­thing that could dra­mat­i­cal­ly change the func­tion of the virus), there were two amino acid changes they iden­ti­fied. That’s what defined the Type A, B, and C strains: Type B stains all have a genet­ic muta­tion that results in an an amino acid muta­tion and Type C has an addi­tion­al amino acid change from Type B (so Type C has two amino acid dif­fer­ences from Type A). Type A is the ‘orig­i­nal’ strain that ini­tial­ly caused the out­break in Chi­na. Type B popped up in Wuhan, quick­ly becom­ing the dom­i­nant strain there sug­gest­ing that Type B may be bet­ter at out­com­pet­ing Type A. And Type C emerged from Type B in Sin­ga­pore. Europe was pri­mar­i­ly hit by Types B and C. And the only coun­tries with sig­nif­i­cant infec­tions of Type A out­side of Chi­na are the US and Aus­tralia, with the US West Coast cas­es being dom­i­nat­ed by Type A strains while New York City and the East Coast are pri­mar­i­ly Type B strains.

    Next, recall how the Cam­bridge team esti­mat­ed the date range for the emer­gence of Type A in Chi­na can came up with a range of Sep­tem­ber 13 — Decem­ber 7, which has the last week of Octo­ber right in the mid­dle. It was that last week in Octo­ber that we had the Mil­i­tary World Games in Wuhan, lead­ing to counter accu­sa­tions by the Chi­nese gov­ern­ment that the virus was intro­duced to Chi­na by the US mil­i­tary at those games, although tech­ni­cal­ly any mil­i­tary attend­ing those games could be a pos­si­ble source of the virus under that sce­nario. Or real­ly any inde­pen­dent group with access to the virus. All you’d have to do is infect some sol­diers.

    Next, recall the pos­si­ble impli­ca­tions if there were indeed infect­ed sol­diers at the Mil­i­tary World Games: if those sol­diers brought the virus back to their mil­i­tary bases or home coun­tries in late October/early Novem­ber and the virus start­ed spread­ing local­ly, that would raise the pos­si­bil­i­ty that there are strains of Type A float­ing around that DON’T have the same muta­tions that were acquired by Type A in Wuhan before jump­ing to the US in late 2019. In oth­er words, strains that don’t ‘fit’ into any of the exist­ing fam­i­ly trees of the virus.

    Remem­ber, we are told that the virus emerged in Wuhan as the orig­i­nal Type A and then spread around for a while acquir­ing new muta­tions (so a bunch of Type A sub­types were emerg­ing) until the Type B strain evolved in Wuhan — which has an amino acid dif­fer­ence from Type A and there­fore might be func­tion­al­ly dif­fer­ent — and the pan­dem­ic sud­den­ly explod­ed as Type B soon become the dom­i­nant strain in Wuhan. At some point while this was hap­pen­ing the first Type A strain made its way to the US from Chi­na ans start­ed spread­ing along the US West Coast. And when that Type A strain first arrived it should have had any muta­tions that had pre­vi­ous­ly been acquired in Wuhan and there­fore all of the oth­er cas­es of Type A in the US should have those same ear­ly-Wuhan muta­tions if we assume that is the ori­gin of the US cas­es of Type A.

    But if the US actu­al­ly got Type A ear­li­er from infect­ed sol­diers (or per­haps an escaped virus from Fort Det­rick), there could be phy­lo­ge­net­ic fam­i­ly trees of Type A sub­types in the US that don’t have those ear­ly Wuhan muta­tions. They would, instead, have what­ev­er muta­tions were ran­dom­ly acquired as the Type A strain spread around the mil­i­tary base a local com­mu­ni­ty. And if these alter­na­tive Type A familes of relat­ed sub­types were sequenced and sub­mit­ted to a sequence data­base like GISAID they would stick out like a sore thumb to ana­lysts and raise major ques­tions about when and how the virus arrived in the US (or Aus­tralia or any oth­er coun­try that may have had an ear­li­er infec­tion). So if a gov­ern­ment was heav­i­ly invest­ed in the cur­rent pre­vail­ing nar­ra­tive — that the virus erupt­ed in Chi­na in late 2019 and only spread around the world start­ing in Decem­ber — that gov­ern­ment would need to avoid the dis­cov­ery of any alter­na­tive Type A phy­lo­ge­net­ic trees that chal­lenge that nar­ra­tive.

    Final­ly, recall that since the Type B strain appeared to com­plete­ly over­take Type A when it emerged in Wuhan that sug­gests Type B might be able to out­com­pete Type A when they are both spread­ing in the same loca­tion and there­fore one of the most effec­tive ways to avoid the dis­cov­ery of alter­na­tive Type A phy­lo­ge­net­ic trees would sim­ply be to do an inad­e­quate job of con­trol­ling the pan­dem­ic so it con­tin­ues to spread thus allow the dom­i­nant Type B strains to move into the areas where any alter­na­tive Type A phy­lo­ge­net­ic strains might be float­ing around and become the dom­i­nant strain most like­ly to be sequenced. That’s part of the con­text of the GOP/Koch/Mercer/militia Tea Par­ty-style cam­paign to clam­or for reopen­ing states: the states that are reopen­ing as a con­se­quence of those protests are the states that have had the fewest cas­es dis­cov­ered and there­fore are the most under­sam­pled states when it comes to the viral sequences float­ing around in them. So if states reopen too soon the Type B strain from the East Coast is bound to sweep in and dom­i­nate new cas­es after the inevitable ‘sec­ond wave’ of new cas­es.

    That’s all the con­text for fol­low­ing sto­ry. A sto­ry about a recent deci­sion by Pres­i­dent Trump that threat­ens to spread that Type B strain not only all over the US but in par­tic­u­lar all across the US mil­i­tary, the insti­tu­tion most like­ly to be har­bor­ing alter­na­tive Type A phy­lo­ge­net­ic strains that could have been cir­cu­lat­ing unde­tect­ed for who knows how long in that rel­a­tive­ly young and healthy demo­graph­ic: Trump just made a sur­prise announce­ment that he’s going to be giv­ing the com­mence­ment address for the grad­u­at­ing West Point class on June 13th. Just 6 weeks away. In New York City. The heart of the Type B pan­dem­ic in the US

    Pres­i­dent Trump’s announce­ment report­ed­ly caught Army offi­cials com­plete­ly off guard, who now have to scram­ble to devel­op plans for call­ing the ~1,000 grad­u­at­ing cadets who have already scat­tered across the coun­try back to New York City for the cer­e­mo­ny before going back home and hope­ful­ly not spread­ing the virus. It real­ly was like the per­fect move if spread­ing Type B across the mil­i­tary and US was a goal. These young cadets are the most like­ly to be asymp­to­matic spread­ers who can spread it to all sorts of oth­er young healthy peo­ple capa­ble of asymp­to­matic spread. Even if 999 of the cadets suc­cess­ful go through this with­out catch­ing the dis­ease and spread­ing it around, a sin­gle case get­ting through the mil­tary’s COVID sur­veil­lance regime could be enough to set off a new wave in the mil­i­tary. A new Type B wave in the mil­i­tary that could over­take any old­er Type A strains that peo­ple may not want dis­cov­ered:

    The New York Times

    Trump Speech to Bring 1,000 West Point Cadets Back to Cam­pus

    The president’s off-again, on-again speech in June will bring back cadets who had scat­tered across the coun­try to help counter the coro­n­avirus.

    By Eric Schmitt and Annie Karni
    April 24, 2020

    WASHINGTON — For Pres­i­dent Trump, who adores the pomp and pre­ci­sion of mil­i­tary cer­e­monies, this was the year he would final­ly get one of the spe­cial perks of being pres­i­dent — deliv­er­ing the com­mence­ment address at West Point, the only ser­vice acad­e­my where he has not spo­ken.

    But the grad­u­a­tion was post­poned because of the coro­n­avirus, the cadets were sent home and offi­cials at the school were not sure when it would be held or even whether it was a good idea to hold it.

    The Naval Acad­e­my, for its part, decid­ed it was too risky to recall its near­ly 1,000 grad­u­at­ing mid­ship­men to Annapo­lis, Md., for a com­mence­ment. Those grad­u­ates will have a vir­tu­al event. But the Air Force Acad­e­my, in con­trast to the oth­er schools, sent home its under­class­men, locked down its seniors on cam­pus, moved up grad­u­a­tion, man­dat­ed social dis­tanc­ing — and went ahead with plans for Vice Pres­i­dent Mike Pence to be its speak­er.

    And so last Fri­day, the day before Mr. Pence was to speak at the Air Force cer­e­mo­ny in Col­orado, Mr. Trump, nev­er one to be upstaged, abrupt­ly announced that he would, in fact, be speak­ing at West Point.

    That was news to every­one, includ­ing offi­cials at West Point, accord­ing to three peo­ple involved with or briefed on the event. The acad­e­my had been look­ing at the option of a delayed pres­i­den­tial com­mence­ment in June, but had yet to com­plete any plans. With Mr. Trump’s pre-emp­tive state­ment, they are now sum­mon­ing 1,000 cadets scat­tered across the coun­try to return to cam­pus in New York, the state that is the cen­ter of the out­break.

    “He’s the com­man­der in chief, that’s his call,” said Sue Ful­ton, a West Point grad­u­ate and for­mer chair­woman of the academy’s Board of Vis­i­tors. “Cadets are cer­tain­ly excit­ed about the oppor­tu­ni­ty to have some­thing like the clas­sic grad­u­a­tion, stand­ing togeth­er, fling­ing their hats in the air.

    “But every­one is leery about bring­ing 1,000 cadets into the New York met­ro­pol­i­tan area for a cer­e­mo­ny,” she added. “It’s def­i­nite­ly a risk.”

    Mr. Trump, like some of his pre­de­ces­sors, has used the annu­al com­mence­ment address­es at the country’s mil­i­tary acad­e­mies to pro­mote his for­eign pol­i­cy suc­cess­es and project strength, some­thing he needs to do in the mid­dle of a pan­dem­ic that has kept him in the White House in the mid­dle of an elec­tion year.

    There will nev­er be a bet­ter set­ting for the pres­i­dent to talk up the size and abil­i­ties of the Unit­ed States mil­i­tary, and point to the uni­formed ranks in front of him as exam­ples of the patri­ot­ic Amer­i­cans he has enlist­ed to fight the coro­n­avirus and car­ry out his cam­paign promise from 2016 of win­ning “so much you’re going to get tired of win­ning.”

    Mr. Trump, who was so impressed by the Bastille Day parade he saw in Paris that he planned some­thing sim­i­lar in Wash­ing­ton until the Pen­ta­gon esti­mat­ed its cost, basks in the glow of the spit-and-pol­ish com­mence­ment cer­e­monies at the mil­i­tary acad­e­mies.

    He spoke at Annapo­lis in 2018, and when he addressed the Air Force Acad­e­my grad­u­a­tion last year, the pres­i­dent stayed and shook hands with all 1,000 cadets. But it is West Point that holds spe­cial sig­nif­i­cance to Mr. Trump, aides said. A grad­u­ate of the New York Mil­i­tary Acad­e­my, he looks upon the West Point grad­u­ates serv­ing in his admin­is­tra­tion with the same admi­ra­tion he has for any­one with Ivy League cre­den­tials.

    It had been a long­stand­ing plan that the pres­i­dent would deliv­er the com­mence­ment speech there in late May, White House offi­cials said, adding that after the event was post­poned, they were still in talks with the acad­e­my about find­ing a new date.

    White House offi­cials said Mr. Trump left it up to the school to decide whether it was safe to hold a grad­u­a­tion cer­e­mo­ny in June, and point­ed out that he could always reassess his deci­sion clos­er to the date if the coro­n­avirus cri­sis made it impos­si­ble for him to attend.

    But his appear­ance at West Point, while not in any way unusu­al or unex­pect­ed, had yet to be announced.

    Indeed, after all the West Point cadets were sent home for spring break in March, Lt. Gen. Dar­ryl A. Williams, the West Point super­in­ten­dent, ordered a work­ing group there to draw up options — much like a bat­tle cam­paign — for what to do about grad­u­a­tion, sum­mer train­ing and ini­ti­a­tion day for incom­ing cadets.

    One option includ­ed a delayed pres­i­den­tial com­mence­ment speech in mid-June, but noth­ing had been decid­ed, acad­e­my offi­cials said.

    That is, noth­ing had been decid­ed until last Fri­day, April 17, when, at a news con­fer­ence, Mr. Trump was asked about Mr. Pence’s com­ing trip to the Air Force Acad­e­my in Col­orado Springs.

    Mr. Trump told reporters that he would be speak­ing at the West Point grad­u­a­tion in the near future, not­ing that he did not like the look of a social­ly dis­tanced grad­u­a­tion and that he hoped the “look” of the cer­e­mo­ny would be “nice and tight.” He did not announce a date for the event.

    West Point offi­cials said this week that they were tak­en aback by the impromp­tu announce­ment. Of the many grad­u­a­tion options under review, Mr. Trump had pre-empt­ed their plan­ning.

    A White House offi­cial said that the admin­is­tra­tion had been in dis­cus­sions with West Point about a new date for the grad­u­a­tion, and that the acad­e­my had offered June 13 as a pos­si­bil­i­ty.

    On the morn­ing of April 18, White House offi­cials said, Mr. Trump had a dis­cus­sion with the Defense Depart­ment, in which he con­firmed that he would speak at West Point on June 13.

    At a news con­fer­ence lat­er that day, Mr. Trump pub­licly announced the date for the first time. “I’m going to West Point. I think they’re chang­ing the date to June 13th because of what’s going on in New York,” he said. “They’re mov­ing into June 13th. West Point.”

    In a state­ment, a White House offi­cial said that “the pres­i­dent had spo­ken with D.O.D. and his remarks on that Sat­ur­day were not a sur­prise to the acad­e­my.”

    By Wednes­day, the acad­e­my had caught up to the president’s announce­ment. “We are hon­ored to host the com­man­der in chief as we cel­e­brate the many accom­plish­ments of our grad­u­at­ing class,” Gen­er­al Williams said in a state­ment.

    West Point offi­cials say the size and scope of the cer­e­mo­ny will be deter­mined “by safe­ty con­sid­er­a­tions for cadets and the entire West Point com­mu­ni­ty.” Acad­e­my offi­cials say they have not yet decid­ed whether par­ents or oth­er vis­i­tors will be allowed to attend.

    Gen­er­al Williams said in a tele­phone inter­view that return­ing seniors would be test­ed off-cam­pus for the coro­n­avirus. Those who test neg­a­tive will then be sent to the school, where they will be mon­i­tored for 14 days before grad­u­a­tion. While the cam­pus has enough dor­mi­to­ry rooms for the 1,000 seniors, Gen­er­al Williams said that he was still decid­ing whether seniors would share bed­rooms on their return.

    “All 1,000 of them will not inter­mix,” he said. “They’ll be in their rooms. They’ll have their masks on. Groups will be seg­re­gat­ed in the mess hall when they eat.”

    Some fac­ul­ty say this is not only incon­ve­nient to cadets, but it is also a risk to their men­tal well-being. It has been an aca­d­e­m­ic year marred by tragedy even before the out­break. One cadet was killed and 21 oth­ers injured last June after a mil­i­tary vehi­cle over­turned en route to a train­ing exer­cise near the acad­e­my. In Octo­ber, a cadet killed him­self.

    Gen­er­al Williams, who man­aged the ini­tial stages of the Amer­i­can mil­i­tary response to the Ebo­la pan­dem­ic in Liberia in 2014, said that he was draw­ing from his expe­ri­ences dur­ing that out­break. He spent three weeks in quar­an­tine in Italy after return­ing from Liberia dur­ing Ebo­la, and said he planned to use some of what he had learned dur­ing his own iso­la­tion to help return­ing West Point seniors.

    “I’m not wait­ing for them to come back here to start wor­ry­ing about their men­tal health,” he said.

    Since leav­ing cam­pus in March, a hand­ful of the academy’s 4,400 cadets have test­ed pos­i­tive for the coro­n­avirus, and about 30 staff and fac­ul­ty mem­bers have test­ed pos­i­tive, said Lt. Col. Christo­pher Ophardt, an acad­e­my spokesman.

    Grad­u­at­ing seniors, known as “firsties,” would have had to come back at some point to take final exams, pack up their belong­ings and out-process, some said.

    “If receiv­ing their diplo­ma and, most impor­tant­ly, their com­mis­sion with POTUS can top off that week, then my feel­ing is that all grad­u­ates would sup­port it,” said Michael J. Meese, a retired one-star Army gen­er­al who taught at West Point and served on Mr. Trump’s tran­si­tion team, using the acronym for the pres­i­dent of the Unit­ed States.

    West Point still has to clear a few more hur­dles to real­ize Mr. Trump’s wish. The acad­e­my has asked Defense Sec­re­tary Mark T. Esper for waivers from a ban on trav­el for mil­i­tary per­son­nel that runs through June 30, to allow cadets to return from all over the coun­try.

    ...

    ———-

    “Trump Speech to Bring 1,000 West Point Cadets Back to Cam­pus” by Eric Schmitt and Annie Karni; The New York Times; 04/24/2020

    That was news to every­one, includ­ing offi­cials at West Point, accord­ing to three peo­ple involved with or briefed on the event. The acad­e­my had been look­ing at the option of a delayed pres­i­den­tial com­mence­ment in June, but had yet to com­plete any plans. With Mr. Trump’s pre-emp­tive state­ment, they are now sum­mon­ing 1,000 cadets scat­tered across the coun­try to return to cam­pus in New York, the state that is the cen­ter of the out­break.”

    What a grand sur­prise from the pres­i­dent: a sur­prise order to call 1,000 cadets scat­tered across the coun­try to the cen­ter of the out­break for a big cer­e­mo­ny on June 13th at the West Point cam­pus that’s only about 50 miles North of New York City. And then they’ll all rescat­ter back across the coun­try to share any new infec­tions. And if you’re expect­ing to see a bunch of cadets social­ly dis­tanced with face masks, note how Trump said he did­n’t like the look of oth­er social­ly dis­tanced mil­i­tary grad­u­a­tion cer­e­monies and hoped the “look” would be “nice and tight”:

    ...
    Mr. Trump told reporters that he would be speak­ing at the West Point grad­u­a­tion in the near future, not­ing that he did not like the look of a social­ly dis­tanced grad­u­a­tion and that he hoped the “look” of the cer­e­mo­ny would be “nice and tight.” He did not announce a date for the event.

    West Point offi­cials said this week that they were tak­en aback by the impromp­tu announce­ment. Of the many grad­u­a­tion options under review, Mr. Trump had pre-empt­ed their plan­ning.

    A White House offi­cial said that the admin­is­tra­tion had been in dis­cus­sions with West Point about a new date for the grad­u­a­tion, and that the acad­e­my had offered June 13 as a pos­si­bil­i­ty.

    ...

    West Point still has to clear a few more hur­dles to real­ize Mr. Trump’s wish. The acad­e­my has asked Defense Sec­re­tary Mark T. Esper for waivers from a ban on trav­el for mil­i­tary per­son­nel that runs through June 30, to allow cadets to return from all over the coun­try.
    ...

    And, again, New York isn’t just the cen­ter of the out­break in the US. It’s the cen­ter of the Type B strain out­break in the US mean­ing when those stu­dents rescat­ter back across the US they’re going to be rescat­ter­ing Type B strains. Which is exact­ly what one would want to hap­pen if they want­ed to obscure non-Chi­na-ori­gin Type A phy­lo­ge­net­ic strains that could be silent­ly spread­ing in the parts of the US.

    Now, here’s an arti­cle about new research that relates to this ‘let Type B sweep over old­er Type A’ sce­nario. It also just more gen­er­al­ly relates to our under­stand­ing of the nature of this dis­ease in cru­cial ways: A research team led by Pro­fes­sor Li Lan­juan at Zhe­jiang Uni­ver­si­ty just devel­oped a test to com­pare the infec­tiv­i­ty of dif­fer­ent strains of the virus. Dr. Li was the per­son who first called for the lock­down of Wuhan so this is some­one who has been at the fore­front of under­stand­ing this virus from the begin­ning.

    The team ran­dom­ly sam­pled 11 strains found with­in Chi­na, infect­ed live cells with the virus, and mea­sured the lev­el of virus at dif­fer­ent time points. They found a sig­nif­i­cant dif­fer­ence in viral lev­els, with a ~270-fold dif­fer­ence between the ‘strongest’ and ‘weak­est’ of the 11 test­ed strains. They also found quite a few pre­vi­ous­ly undis­cov­ered muta­tions which sug­gests there’s a sig­nif­i­cant under­sam­pling of viral sequences right now.

    Cru­cial­ly, they found that the ‘stronger’ strains that pro­duced high­er viral loads were the strains that went on to pre­dom­i­nant­ly infect Europe and then the East Coast of the US and that this may account for the dif­fer­ent mor­tal­i­ty rates observed between the US East Coast and West Coast. Recall how Dr. Forster’s found that the Type B and Type C strains went on to dom­i­nate the Euro­pean and US East Coast infec­tions. Also recall how the Type A and Type B strains appears to cor­re­spond to ‘S‑Type’ and ‘L‑Type’ strains iden­ti­fied by an ear­li­er team out of Chi­na. That team observed that the ‘L‑Type’ strain emerged in Wuhan from the ear­li­er ‘S‑Type’ type and then went on to almost entire­ly dom­i­nate the new cas­es in the city, lead­ing the team to spec­u­late that the L‑Type strain real­ly was some­how more vir­u­lent. This prompt­ed oth­er virol­o­gist to attack the team’s find­ings for sug­gest­ing that there might be a func­tion­al dif­fer­ence between the S and L‑types because there were oth­er pos­si­ble expla­na­tions for why the L‑Type sud­den­ly came to dom­i­nate new cas­es. Well, based on this lat­est research it sure sounds like the L‑type (Type B) strain real­ly is more vir­u­lent than the S‑type (Type A) strain. So by call­ing back those 1000 cadets to attend Trump’s West Point cer­e­mo­ny in June there isn’t just going to be a spread of the virus across the US and inside the mil­i­tary. It’s going to be the spread of the dead­lier strains of the virus:

    South Chi­na Morn­ing Post

    Coronavirus’s abil­i­ty to mutate has been vast­ly under­es­ti­mat­ed, and muta­tions affect dead­li­ness of strains, Chi­nese study finds

    * The most aggres­sive strains of Sars-CoV­‑2 could gen­er­ate 270 times as much viral load as the least potent type
    * New York may have a dead­lier strain import­ed from Europe, com­pared to less dead­ly virus­es else­where in the Unit­ed States

    Stephen Chen in Bei­jing
    Pub­lished: 10:41pm, 20 Apr, 2020

    A new study by one of China’s top sci­en­tists has found the abil­i­ty of the new coro­n­avirus to mutate has been vast­ly under­es­ti­mat­ed and dif­fer­ent strains may account for dif­fer­ent impacts of the dis­ease in var­i­ous parts of the world.

    Pro­fes­sor Li Lan­juan and her col­leagues from Zhe­jiang Uni­ver­si­ty found with­in a small pool of patients many muta­tions not pre­vi­ous­ly report­ed. These muta­tions includ­ed changes so rare that sci­en­tists had nev­er con­sid­ered they might occur.

    They also con­firmed for the first time with lab­o­ra­to­ry evi­dence that cer­tain muta­tions could cre­ate strains dead­lier than oth­ers.

    “Sars-CoV­‑2 has acquired muta­tions capa­ble of sub­stan­tial­ly chang­ing its path­o­genic­i­ty,” Li and her col­lab­o­ra­tors wrote in a non-peer reviewed paper released on preprint ser­vice medRxiv.org on Sun­day.

    Li’s study pro­vid­ed the first hard evi­dence that muta­tion could affect how severe­ly the virus caused dis­ease or dam­age in its host.

    Li took an unusu­al approach to inves­ti­gate the virus muta­tion. She analysed the viral strains iso­lat­ed from 11 ran­dom­ly cho­sen Covid-19 patients from Hangzhou in the east­ern province of Zhe­jiang, and then test­ed how effi­cient­ly they could infect and kill cells.

    The dead­liest muta­tions in the Zhe­jiang patients had also been found in most patients across Europe, while the milder strains were the pre­dom­i­nant vari­eties found in parts of the Unit­ed States, such as Wash­ing­ton state, accord­ing to their paper.

    A sep­a­rate study had found that New York strains had been import­ed from Europe. The death rate in New York was sim­i­lar to that in many Euro­pean coun­tries, if not worse.

    But the weak­er muta­tion did not mean a low­er risk for every­body, accord­ing to Li’s study. In Zhe­jiang, two patients in their 30s and 50s who con­tract­ed the weak­er strain became severe­ly ill. Although both sur­vived in the end, the elder patient need­ed treat­ment in an inten­sive care unit.

    This find­ing could shed light on dif­fer­ences in region­al mor­tal­i­ty. The pandemic’s infec­tion and death rates vary from one coun­try to anoth­er, and many expla­na­tions have been pro­posed.

    Genet­ic sci­en­tists had noticed that the dom­i­nant strains in dif­fer­ent geo­graph­ic regions were inher­ent­ly dif­fer­ent. Some researchers sus­pect­ed the vary­ing mor­tal­i­ty rates could, in part, be caused by muta­tions but they had no direct proof.

    The issue was fur­ther com­pli­cat­ed because sur­vival rates depend­ed on many fac­tors, such as age, under­ly­ing health con­di­tions or even blood type.

    In hos­pi­tals, Covid-19 has been treat­ed as one dis­ease and patients have received the same treat­ment regard­less of the strain they have. Li and her col­leagues sug­gest­ed that defin­ing muta­tions in a region might deter­mine actions to fight the virus.

    “Drug and vac­cine devel­op­ment, while urgent, need to take the impact of these accu­mu­lat­ing muta­tions … into account to avoid poten­tial pit­falls,” they said.

    Li was the first sci­en­tist to pro­pose the Wuhan lock­down, accord­ing to state media reports. The gov­ern­ment fol­lowed her advice and in late Jan­u­ary, the city of more than 11 mil­lion res­i­dents was shut down overnight.

    The sam­ple size in this most recent study was remark­ably small. Oth­er stud­ies track­ing the virus muta­tion usu­al­ly involved hun­dreds, or even thou­sands, of strains.

    Li’s team detect­ed more than 30 muta­tions. Among them 19 muta­tions – or about 60 per cent – were new.

    They found some of these muta­tions could lead to func­tion­al changes in the virus’ spike pro­tein, a unique struc­ture over the viral enve­lope enabling the coro­n­avirus to bind with human cells. Com­put­er sim­u­la­tion pre­dict­ed that these muta­tions would increase its infec­tiv­i­ty.

    To ver­i­fy the the­o­ry, Li and col­leagues infect­ed cells with strains car­ry­ing dif­fer­ent muta­tions. The most aggres­sive strains could gen­er­ate 270 times as much viral load as the weak­est type. These strains also killed the cells the fastest.

    It was an unex­pect­ed result from few­er than a dozen patients, “indi­cat­ing that the true diver­si­ty of the viral strains is still large­ly under­ap­pre­ci­at­ed,” Li wrote in the paper.

    The muta­tions were genes dif­fer­ent from the ear­li­est strain iso­lat­ed in Wuhan, where the virus was first detect­ed in late Decem­ber last year.

    The coro­n­avirus changes at an aver­age speed of about one muta­tion per month. By Mon­day, more than 10,000 strains had been sequenced by sci­en­tists around the globe, con­tain­ing more than 4,300 muta­tions, accord­ing to the Chi­na Nation­al Cen­tre for Bioin­for­ma­tion.

    Most of these sam­ples, though, were sequenced by a stan­dard approach that could gen­er­ate a result quick­ly. The genes were read just once, for instance, and there was room for mis­takes.

    Li’s team used a more sophis­ti­cat­ed method known as ultra-deep sequenc­ing. Each build­ing block of the virus genome was read more than 100 times, allow­ing the researchers to see changes that could have been over­looked by the con­ven­tion­al approach.

    The researchers also found three con­sec­u­tive changes – known as tri-nucleotide muta­tions – in a 60-year-old patient, which was a rare event. Usu­al­ly the genes mutat­ed at one site at a time. This patient spent more than 50 days in hos­pi­tal, much longer than oth­er Covid-19 patients, and even his fae­ces were infec­tious with liv­ing viral strains.

    “Inves­ti­gat­ing the func­tion­al impact of this tri-nucleotide muta­tion would be high­ly inter­est­ing,” Li and col­leagues said in the paper.

    ...

    ———–

    “Coronavirus’s abil­i­ty to mutate has been vast­ly under­es­ti­mat­ed, and muta­tions affect dead­li­ness of strains, Chi­nese study finds” by Stephen Chen; South Chi­na Morn­ing Post; 04/20/2020

    “They also con­firmed for the first time with lab­o­ra­to­ry evi­dence that cer­tain muta­tions could cre­ate strains dead­lier than oth­ers.”

    It’s the first val­i­da­tion that there real­ly are dif­fer­ent strains with dif­fer­ent lev­els of mor­tal­i­ty. A 270-fold dif­fer­ence in observed viral lev­els between the strongest and weak­est strains. And this dra­mat­ic dif­fer­ence was dis­cov­ered from just a tiny sam­ple of 11 ran­dom­ly select­ed strains, hint­ing at poten­tial­ly more sig­nif­i­cant dif­fer­ences between strains that have yet to be dis­cov­ered:

    ...
    Li took an unusu­al approach to inves­ti­gate the virus muta­tion. She analysed the viral strains iso­lat­ed from 11 ran­dom­ly cho­sen Covid-19 patients from Hangzhou in the east­ern province of Zhe­jiang, and then test­ed how effi­cient­ly they could infect and kill cells.

    The dead­liest muta­tions in the Zhe­jiang patients had also been found in most patients across Europe, while the milder strains were the pre­dom­i­nant vari­eties found in parts of the Unit­ed States, such as Wash­ing­ton state, accord­ing to their paper.

    ...

    They found some of these muta­tions could lead to func­tion­al changes in the virus’ spike pro­tein, a unique struc­ture over the viral enve­lope enabling the coro­n­avirus to bind with human cells. Com­put­er sim­u­la­tion pre­dict­ed that these muta­tions would increase its infec­tiv­i­ty.

    To ver­i­fy the the­o­ry, Li and col­leagues infect­ed cells with strains car­ry­ing dif­fer­ent muta­tions. The most aggres­sive strains could gen­er­ate 270 times as much viral load as the weak­est type. These strains also killed the cells the fastest.

    It was an unex­pect­ed result from few­er than a dozen patients, “indi­cat­ing that the true diver­si­ty of the viral strains is still large­ly under­ap­pre­ci­at­ed,” Li wrote in the paper.
    ...

    And not only could these find­ings help explain dif­fer­ences in region­al mor­tal­i­ty (e.g. why the pan­dem­ic was so much worse on US East Coast than West Coast), but it could also have impli­ca­tions for the devel­op­ment of a vac­cine. One of the dis­turb­ing aspects of this virus from the begin­ning has been the rel­a­tive­ly low muta­tion rates, espe­cial­ly for muta­tions that make a func­tion­al dif­fer­ence in the virus, because that reflect­ed how the virus was already so incred­i­bly well-evolved for spread­ing between humans. But the one ben­e­fit of that near-opti­mized evo­lu­tion­ary sta­tus was the prospects of eas­i­er vac­cine devel­op­ment that would­n’t have to wor­ry as much about a chang­ing virus neu­tral­iz­ing the vac­cine. This study is a hint that we still might run into com­pli­ca­tions from a chang­ing virus when devel­op­ing a vac­cine despite the virus already being so remark­ably effi­cient at spread­ing:

    ...
    This find­ing could shed light on dif­fer­ences in region­al mor­tal­i­ty. The pandemic’s infec­tion and death rates vary from one coun­try to anoth­er, and many expla­na­tions have been pro­posed.

    Genet­ic sci­en­tists had noticed that the dom­i­nant strains in dif­fer­ent geo­graph­ic regions were inher­ent­ly dif­fer­ent. Some researchers sus­pect­ed the vary­ing mor­tal­i­ty rates could, in part, be caused by muta­tions but they had no direct proof.

    The issue was fur­ther com­pli­cat­ed because sur­vival rates depend­ed on many fac­tors, such as age, under­ly­ing health con­di­tions or even blood type.

    In hos­pi­tals, Covid-19 has been treat­ed as one dis­ease and patients have received the same treat­ment regard­less of the strain they have. Li and her col­leagues sug­gest­ed that defin­ing muta­tions in a region might deter­mine actions to fight the virus.

    “Drug and vac­cine devel­op­ment, while urgent, need to take the impact of these accu­mu­lat­ing muta­tions … into account to avoid poten­tial pit­falls,” they said.
    ...

    Bit by bit, the pic­ture that’s emerg­ing real­ly is increas­ing­ly look­ing like the virus real­ly has got­ten dead­lier as the pan­dem­ic evolved. But not dead­lier due to an enhanced abil­i­ty to infect human cells. The virus is already incred­i­bly good at that. Instead, it’s look­ing like the dead­lier strains are are some­how bet­ter at mak­ing viral copies after infec­tion and a great way to infect more peo­ple is to make more copies of the virus. This is an impor­tant point regard­ing the sce­nario of just allow­ing Type B cas­es to sweep over areas that could have old­er alter­na­tive Type A strains because it adds fur­ther evi­dence that Type B real­ly is bet­ter at out­com­pet­ing Type A when they’re in the same loca­tion. So if indeed there real­ly is an agen­da of allow­ing more aggres­sive strains from Europe to sweep over regions of the US where old­er alter­na­tive Type A strains could be float­ing around this lat­est research sug­gests that agen­da has a good chance of work­ing. Work­ing by spread­ing an extra dead­ly ver­sion of the virus around.

    Posted by Pterrafractyl | April 29, 2020, 12:35 pm
  3. In light of the wide­spread and seem­ing­ly blind ongo­ing accep­tance of the ‘expert’ con­clu­sion that there is strong evi­dence that the SARS-CoV­‑2 virus was­n’t man-made, here’s a pair of inter­views with oth­er experts who are thank­ful­ly sup­ply­ing sane rebut­tals to that absurd con­clu­sion. Both inter­views address that let­ter to Nature pub­lished on March 17 by Kris­t­ian G. Ander­son, et al., where they made a sur­pris­ing­ly shod­dy case for why the virus could­n’t have been man-made. A let­ter which was sud­den­ly and wide­ly tout­ed as some sort of defin­i­tive answer to the ques­tion:

    First, here’s an inter­view of Pro­fes­sor Stu­art New­man, pro­fes­sor of cell biol­o­gy and anato­my at New York Med­ical Col­lege, did with GMWatch, a UK based non-prof­it focused on genet­i­cal­ly mod­i­fied foods. Pro­fes­sor New­man is a strong crit­ic of the biotech­nol­o­gy indus­try being applied to agri­cul­ture. The sec­ond inter­view is with Dr Michael Anto­niou, anoth­er long-time crit­ic of GMO tech­nol­o­gy. So we have two long-stand­ing GMO crit­ics who have a a lot of expe­ri­ence pub­licly call­ing BS on mis­guid­ed con­sen­sus views now call­ing BS on that wide­spread blind embrace of that Nature let­ter.

    So how does New­man rebut that Nature let­ter? Well, for starters, he address­es the key argu­ment in the Nature let­ter about the SARS-CoV­‑2 virus’s Recep­tor Bind­ing Domain (RBD). That was the argu­ment that because the sequence for the RBD did­n’t exact­ly match the “opti­mized” RBD that sim­u­la­tions used by some experts pre­dict would be the opti­mal design for max­i­mum bind­ing to the ACE2 recep­tor there­fore the virus was very like­ly not man-made. This is a sil­ly argu­ment for a num­ber of rea­sons, includ­ing the obvi­ous fact that some­one design­ing a virus might want it to look like a designed virus and might not need it to have the max­i­mum the­o­ret­i­cal recep­tor bind­ing capac­i­ty and the fact that tech­niques for undi­rect­ed evo­lu­tion that could find­ing pre­vi­ous­ly unknown sequences with enhanced bind­ing are well estab­lished tech­niques. But as New­man points outs, while the par­tic­u­lar RBD sim­u­la­tions referred to by those authors may have arrived at a dif­fer­ent RBD sequence than what we find in SARS-CoV­‑2, the RBD of SARS has been close­ly stud­ied by labs around the world for decades. How many dif­fer­ent “opti­mized” sequences for that RBD have been found in those years? Who knows, and that’s the point: not only is it absurd to assume that an engi­neered virus would have to have the exact opti­mized RBD sequence they cal­cu­lat­ed in their sim­u­la­tion but it’s absurd to assume there’s only one “opti­mized” RBD sequence that’s been devel­oped in a lab.

    New­man then address­es the sec­ond key argu­ment in the Nature paper about the furin cleav­age site found on the S‑protein that makes it extreme­ly easy for the virus to get acti­vat­ed after bind­ing with an ACE2 recep­tor. Recall how the authors appeared to argue that while a poly­ba­sic cleav­age site like the one found in SARS-CoV­‑2 has­n’t been observed in oth­er bat or pan­golin coro­n­avirus­es — and it’s assumed that the virus came from bats or pan­golins — it’s pos­si­ble the furin cleav­age site could have evolved nat­u­ral­ly, espe­cial­ly if there were a num­ber of repeat­ed ani­mal-to-human trans­mis­sion events over time that gave the virus repeat­ed oppor­tu­ni­ties to evolve such a site. It’s also pos­si­ble that there are bat or pan­golin coro­n­avirus­es that do have furin cleav­age sites and haven’t been dis­cov­ered yet. And while both of those points are tech­ni­cal­ly true, pro­fes­sor New­man points out that adding a furin cleav­age site to coro­n­virus­es to inves­ti­gate how that impacts the virus’s path­o­genic­i­ty is actu­al­ly some­thing that has been done in pub­lished exper­i­ments. Beyond that, they actu­al­ly cite one of those papers in the Nature let­ter and refer to those exper­i­ments. So if we are pred­i­cat­ing our deter­mi­na­tion of whether or not this virus was man-made based on whether or not the virus has fea­tures that have been pre­vi­ous­ly cre­at­ed in the lab as they pro­posed for the enhanced ACE2 bind­ing of the SARS-CoV­‑2 RBD sequence, this furin cleav­age site would indeed be a fea­ture that was pre­vi­ous­ly cre­at­ed in a lab. And yet some­how that just got ignored by the authors despite them cit­ing and men­tion­ing exper­i­ments were furin cleav­age sites were added to coro­n­avirus­es to study them. It’s quite odd.

    In the inter­view with Dr Michael Anto­niou, Anto­niou makes the cru­cial point that when it comes to assess­ing whether or not a virus may have been man-made there’s no need at all to find past research demon­strat­ing the unique opti­mized fea­tures found in your nov­el virus because tech­niques for ran­dom­ly evolv­ing opti­mized fea­tures are well estab­lished. The cre­ators for one such tech­nique won the Nobel prize in 2018. Anto­niou also notes that he wrote a let­ter to Nature Med­i­cine rebut­ting the March 17 let­ter but it was reject­ed on the grounds that “we do not feel that they advance or clar­i­fy under­stand­ing” of the orig­i­nal arti­cle with­out offer­ing a sci­en­tif­ic argu­ment to rebut his points.

    So while a broad and high­ly erro­neous con­sen­sus appears to have emerged that the virus could­n’t pos­si­bly have been man-made, at least that con­sen­sus is being chal­lenged. Chal­lenged and then wide­ly ignored which is why they’re appear­ing niche out­lets like GMWatch. In oth­er words, the goods news is that these chal­lenges are hap­pen­ing. The bad news is that the news is still ignor­ing them:

    GMWatch

    Anoth­er expert chal­lenges asser­tions that SARS-CoV­‑2 was not genet­i­cal­ly engi­neered

    Pub­lished: 27 April 2020

    Anoth­er expert on biotech­nol­o­gy has attacked the evi­dence being used to quash sug­ges­tions that SARS-CoV­‑2, the virus strain that caus­es COVID-19, might have been genet­i­cal­ly engi­neered. Pro­fes­sor Stu­art New­man, pro­fes­sor of cell biol­o­gy and anato­my at New York Med­ical Col­lege, says that a key argu­ment used to deny that it could be a genet­i­cal­ly engi­neered strain that escaped from a lab­o­ra­to­ry actu­al­ly points to the exact oppo­site. In oth­er words, it indi­cates that SARS-CoV­‑2 could well be genet­i­cal­ly engi­neered and that it could have escaped from a lab.

    The evi­dence that is being cit­ed as prov­ing that SARS-CoV­‑2 is “not a lab­o­ra­to­ry con­struct or a pur­pose­ful­ly manip­u­lat­ed virus” is a paper pub­lished by the immu­nol­o­gist Kris­t­ian Ander­sen and col­leagues in Nature Med­i­cine. As Adam Lau­r­ing, an asso­ciate pro­fes­sor of micro­bi­ol­o­gy, immunol­o­gy and infec­tious dis­eases at the Uni­ver­si­ty of Michi­gan Med­ical School, has not­ed, Andersen’s paper argues that, “the SARS-CoV­‑2 virus has some key dif­fer­ences in spe­cif­ic genes rel­a­tive to pre­vi­ous­ly iden­ti­fied coro­n­avirus­es – the ones a lab­o­ra­to­ry would be work­ing with. This con­stel­la­tion of changes makes it unlike­ly that it is the result of a lab­o­ra­to­ry ‘escape’.”

    But Pro­fes­sor New­man says that this is total­ly uncon­vinc­ing because “The ‘key dif­fer­ences’ were in regions of the coro­n­avirus spike pro­tein that were the sub­ject of genet­ic engi­neer­ing exper­i­ments in labs around the world (main­ly in the US and Chi­na) for two decades.”

    So not only does New­man think that the virus could have escaped from a lab, he also thinks that it could have orig­i­nat­ed in a virus stock that had under­gone genet­ic engi­neer­ing at some point.

    In an email inter­view with GMWatch, New­man, who is edi­tor-in-chief of the jour­nal Bio­log­i­cal The­o­ry and co-author (with Tina Stevens) of the book Biotech Jug­ger­naut, ampli­fied this spec­u­la­tion by not­ing, “The Nature Med­i­cine paper points to vari­a­tions in two sites of the spike pro­tein of the new coro­n­avirus that the authors claim must have arisen by nat­ur­al selec­tion in the wild. How­ev­er, genet­ic engi­neer­ing of one of these sites, the ACE2 recep­tor bind­ing domain, has been pro­posed since 2005 in order to help gen­er­ate vac­cines against these virus­es (see this paper). It is puz­zling that the authors of the Nature Med­i­cine com­men­tary did not cite this paper, which appeared in the promi­nent jour­nal Sci­ence.

    More­over, New­man added, “The sec­ond site that Ander­sen et al. assert arose by nat­ur­al means, a tar­get of enzyme cleav­age not usu­al­ly found in this class of virus­es, was in fact intro­duced by genet­ic engi­neer­ing in a sim­i­lar coro­n­avirus in a paper they do cite. This was done to explore mech­a­nisms of path­o­genic­i­ty.

    New­man said that he does not believe that these changes were delib­er­ate­ly intro­duced to increase the path­o­genic­i­ty of any sin­gle strain, but that SARS-CoV­‑2 may have had genet­i­cal­ly engi­neered com­po­nents in its his­to­ry before being inad­ver­tent­ly intro­duced into the human pop­u­la­tion.

    New­man is not the only sci­en­tist that has spo­ken out about the pos­si­bil­i­ty of a genet­i­cal­ly engi­neered ele­ment to the virus. We recent­ly pub­lished an arti­cle in which the mol­e­c­u­lar geneti­cist Dr Michael Anto­niou also cast doubt on asser­tions that the virus was not genet­i­cal­ly engi­neered. Dr Anto­niou set out a method by which the virus could have been genet­i­cal­ly manip­u­lat­ed and select­ed for increased infec­tiv­i­ty in the lab­o­ra­to­ry.

    Nei­ther Dr Anto­niou, nor Prof New­man, nor we our­selves make any sug­ges­tion that, in the event that genet­ic engi­neer­ing was involved, the inten­tion was to cre­ate a bioweapon. Such “enhanced infec­tiv­i­ty” research is car­ried out on virus­es all over the world (and not just in Chi­na) to inves­ti­gate their behav­iour and to devel­op vac­cines and oth­er ther­a­pies, as well as for “biode­fence” pur­pos­es.

    ...

    ———–

    “Anoth­er expert chal­lenges asser­tions that SARS-CoV­‑2 was not genet­i­cal­ly engi­neered”; GMWatch; 04/27/2020

    “In an email inter­view with GMWatch, New­man, who is edi­tor-in-chief of the jour­nal Bio­log­i­cal The­o­ry and co-author (with Tina Stevens) of the book Biotech Jug­ger­naut, ampli­fied this spec­u­la­tion by not­ing, “The Nature Med­i­cine paper points to vari­a­tions in two sites of the spike pro­tein of the new coro­n­avirus that the authors claim must have arisen by nat­ur­al selec­tion in the wild. How­ev­er, genet­ic engi­neer­ing of one of these sites, the ACE2 recep­tor bind­ing domain, has been pro­posed since 2005 in order to help gen­er­ate vac­cines against these virus­es (see this paper). It is puz­zling that the authors of the Nature Med­i­cine com­men­tary did not cite this paper, which appeared in the promi­nent jour­nal Sci­ence.””

    Yep, as far back as 2005 we had papers propos­ing mod­i­fi­ca­tions to the RBD or SARS in order to enhance the bind­ing of the virus. How many the­o­ret­i­cal designs of human coro­n­avirus RBDs have been devel­oped in the fol­low­ing 15 years? And yet the fact that the SARS-CoV­‑2 RBD does­n’t match a par­tic­u­lar sim­u­lat­ed opti­mized RBD gets cit­ed as evi­dence that the virus evolved nat­u­ral­ly. And the same is true with the furin cleav­age site: the addi­tion of a furin cleav­age site to human coro­n­avirus­es has long been pro­posed and they actu­al­ly cite a paper that did exact­ly that. And yet some­how these past exper­i­ments just kind of get dis­missed in their final analy­sis to give way to con­clu­sion that it must have been nat­ur­al:

    ...
    More­over, New­man added, “The sec­ond site that Ander­sen et al. assert arose by nat­ur­al means, a tar­get of enzyme cleav­age not usu­al­ly found in this class of virus­es, was in fact intro­duced by genet­ic engi­neer­ing in a sim­i­lar coro­n­avirus in a paper they do cite. This was done to explore mech­a­nisms of path­o­genic­i­ty.
    ...

    And now here’s the inter­view of Dr Michael Anto­niou, where he makes the cru­cial point when it comes to com­par­ing the observed sequences of virus­es to pre­vi­ous lab exper­i­ments and analy­ses to assess whether or not a virus may have been made in a lab: it makes no sense to expect the fea­tures of an engi­neered virus to match pre­vi­ous­ly engi­neered viral fea­tures because tech­niques the “opti­mized” sequences devel­oped by com­put­er sim­u­la­tions haven’t been val­i­dat­ed in live sys­tems and there are tech­niques for ran­dom­ly devel­op­ing opti­mized viral fea­tures in cell cul­tures and mod­el organ­ism. Direct­ed iter­a­tive evo­lu­tion­ary selec­tion process is an exam­ple of one of these tech­niques: So if some­one uses human cell cul­tures exper­i­ments, for exam­ple, to devel­op a virus opti­mized for infect­ing humans there’s no rea­son to assume the opti­mized viral fea­tures that emerge from those exper­i­ments would match the sim­u­lat­ed the­o­ret­i­cal opti­mized fea­tures:

    GMWatch

    Was the COVID-19 virus genet­i­cal­ly engi­neered?

    by Claire Robin­son
    Pub­lished: 22 April 2020

    Since the COVID-19 pan­dem­ic took off, spec­u­la­tion has been rife about its ori­gins. The truth is that nobody knows for cer­tain how the virus first took hold. But despite that uncer­tain­ty, sug­ges­tions that the virus may have been genet­i­cal­ly engi­neered, or oth­er­wise lab-gen­er­at­ed, have been reject­ed as “con­spir­a­cy the­o­ries” incom­pat­i­ble with the evi­dence.

    Yet the main evi­dence that is cit­ed as end­ing all spec­u­la­tion about the role of genet­ic engi­neer­ing and as prov­ing the virus could only have been the prod­uct of nat­ur­al evo­lu­tion turns out to be sur­pris­ing­ly weak. Let’s take a look at it.

    The authors of a recent­ly pub­lished paper in the jour­nal Nature Med­i­cine argue that the SARS-CoV­‑2 virus dri­ving the pan­dem­ic arose through nat­ur­al muta­tion and selec­tion in ani­mal (notably bats and pan­golins) or human hosts, and not through lab­o­ra­to­ry manip­u­la­tion and acci­den­tal release. And they say they have iden­ti­fied two key char­ac­ter­is­tics of the virus that prove this: the absence of a pre­vi­ous­ly used virus back­bone and the way in which the virus binds to human cells.

    Not the “ide­al” design for infec­tiv­i­ty?

    As you would expect of a virus that can cause a glob­al pan­dem­ic, SARS-CoV­‑2 is good at infect­ing human cells. It does this by bind­ing with high affin­i­ty (that is, it binds strong­ly) to the cell sur­face mem­brane pro­tein known as angiotensin-con­vert­ing enzyme 2 (ACE2), which enables it to enter human cells. But, bas­ing their argu­ment on a com­put­er mod­el­ling sys­tem, the authors of the Nature Med­i­cine paper argue that the inter­ac­tion between the virus and the ACE2 recep­tor is “not ide­al”.

    They say that the recep­tor-bind­ing domain (RBD) amino acid sequence of the SARS-CoV­‑2 spike pro­tein – the part of the spike pro­tein that allows the virus to bind to the ACE2 pro­tein on human cell sur­faces – is dif­fer­ent from those shown in the SARS-CoV fam­i­ly of virus­es to be opti­mal for recep­tor bind­ing.

    They appear to argue, based on their and oth­ers’ com­put­er mod­el­ling data, that they have iden­ti­fied the “ide­al” CoV spike pro­tein RBD amino acid sequence for ACE2 recep­tor bind­ing. They then seem to imply that if you were to genet­i­cal­ly engi­neer SARS-CoV for opti­mal human ACE2 bind­ing and infec­tiv­i­ty, you would use the RBD amino acid sequence pre­dict­ed by their com­put­er mod­el­ling. But they point out that SARS-CoV­‑2 does not have exact­ly the same com­put­er pro­gram-pre­dict­ed RBD amino acid sequence. Thus they con­clude that it could not have been genet­i­cal­ly engi­neered, stat­ing: “This is strong evi­dence that SARS-CoV­‑2 is not the prod­uct of pur­pose­ful manip­u­la­tion.”

    To put it sim­ply, the authors are say­ing that SARS-CoV­‑2 was not delib­er­ate­ly engi­neered because if it were, it would have been designed dif­fer­ent­ly.

    How­ev­er, the Lon­don-based mol­e­c­u­lar geneti­cist Dr Michael Anto­niou com­ment­ed that this line of rea­son­ing fails to take into account that there are a num­ber of lab­o­ra­to­ry-based sys­tems that can select for high affin­i­ty RBD vari­ants that are able to take into account the com­plex envi­ron­ment of a liv­ing organ­ism. This com­plex envi­ron­ment may impact the effi­cien­cy with which the SARS-CoV spike pro­tein can find the ACE2 recep­tor and bind to it. An RBD select­ed via these more real­is­tic real-world exper­i­men­tal sys­tems would be just as “ide­al”, or even more so, for human ACE2 bind­ing than any RBD that a com­put­er mod­el could pre­dict. And cru­cial­ly, it would like­ly be dif­fer­ent in amino acid sequence. So the fact that SARS-CoV­‑2 doesn’t have the same RBD amino acid sequence as the one that the com­put­er pro­gram pre­dict­ed in no way rules out the pos­si­bil­i­ty that it was genet­i­cal­ly engi­neered.

    Lim­its to com­put­er mod­el­ling

    Dr Anto­niou said that the authors’ rea­son­ing is not con­clu­sive because it is based large­ly on com­put­er mod­el­ling, which, he says, is “not defin­i­tive but only pre­dic­tive. It can­not tell us whether any giv­en virus would be opti­mized for infec­tiv­i­ty in a real world sce­nario, such as in the human body. That’s because the envi­ron­ment of the human body will influ­ence how the virus inter­acts with the recep­tor. You can’t mod­el that accu­rate­ly with com­put­er mod­el­ling as there are sim­ply too many vari­ables to fac­tor into the equa­tion.”

    Dr Anto­niou added, “Peo­ple can put too much faith in com­put­er pro­grams, but they are only a begin­ning. You then have to prove whether the com­put­er program’s pre­dic­tion is cor­rect or not by direct exper­i­men­ta­tion in a liv­ing organ­ism. This has not been done in the case of this hypoth­e­sis, so it remains unproven.”

    It is even pos­si­ble that SARS-CoV­‑2 was opti­mized using a liv­ing organ­ism mod­el, result­ing in a virus that is bet­ter at infect­ing humans than any com­put­er mod­el could pre­dict.

    More than one way to engi­neer a virus

    The authors of the Nature Med­i­cine arti­cle seem to assume that the only way to genet­i­cal­ly engi­neer a virus is to take an already known virus and then engi­neer it to have the new prop­er­ties you want. On this premise, they looked for evi­dence of an already known virus that could have been used in the engi­neer­ing of SARS-CoV­‑2.

    And they failed to find that evi­dence. They stat­ed, “Genet­ic data irrefutably show that SARS-CoV­‑2 is not derived from any pre­vi­ous­ly used virus back­bone.”

    But Dr Anto­niou told us that while the authors did indeed show that SARS-CoV­‑2 was unlike­ly to have been built by delib­er­ate genet­ic engi­neer­ing from a pre­vi­ous­ly used virus back­bone, that’s not the only way of con­struct­ing a virus. There is anoth­er method by which an enhanced-infec­tiv­i­ty virus can be engi­neered in the lab.

    A well-known alter­na­tive

    A well-known alter­na­tive process that could have been used has the cum­ber­some name of “direct­ed iter­a­tive evo­lu­tion­ary selec­tion process”. In this case, it would involve using genet­ic engi­neer­ing to gen­er­ate a large num­ber of ran­dom­ly mutat­ed ver­sions of the SARS-CoV spike pro­tein recep­tor bind­ing domain (RBD), which would then be select­ed for strong bind­ing to the ACE2 recep­tor and con­se­quent­ly high infec­tiv­i­ty of human cells.

    This selec­tion can be done either with puri­fied pro­teins or, bet­ter still, with a mix­ture of whole coro­n­avirus (CoV) prepa­ra­tions and human cells in tis­sue cul­ture. Alter­na­tive­ly, the SARS-CoV spike pro­tein vari­ants can be genet­i­cal­ly engi­neered with­in what is known as a “phage dis­play library”. A phage is a virus that infects bac­te­ria and can be genet­i­cal­ly engi­neered to express on its exte­ri­or coat the CoV spike pro­tein with a large num­ber of vari­ants of the RBD. This prepa­ra­tion of phage, dis­play­ing on its sur­face a “library” of CoV spike pro­tein vari­ants, is then added to human cells under lab­o­ra­to­ry cul­ture con­di­tions in order to select for those that bind to the ACE2 recep­tor.

    This process is repeat­ed under more and more strin­gent bind­ing con­di­tions until CoV spike pro­tein vari­ants with a high bind­ing affin­i­ty are iso­lat­ed.

    Once any of the above selec­tion pro­ce­dures for high affin­i­ty inter­ac­tion of SARS-CoV spike pro­tein with ACE2 has been com­plet­ed, then whole infec­tious CoV with these prop­er­ties can be man­u­fac­tured.

    Such a direct­ed iter­a­tive evo­lu­tion­ary selec­tion process is a fre­quent­ly used method in lab­o­ra­to­ry research. So there is lit­tle or no pos­si­bil­i­ty that the Nature Med­i­cine arti­cle authors haven’t heard of it – not least, as it is con­sid­ered so sci­en­tif­i­cal­ly impor­tant that its inven­tors were award­ed the Nobel Prize in Chem­istry in 2018.

    Yet the pos­si­bil­i­ty that this is the way that SARS-CoV­‑2 arose is not addressed by the Nature Med­i­cine arti­cle authors and so its use has not been dis­proven.

    No proof SARS-CoV­‑2 was not genet­i­cal­ly engi­neered

    In sum, the Nature Med­i­cine arti­cle authors offer no evi­dence that the SARS-CoV­‑2 virus could not have been genet­i­cal­ly engi­neered. That’s not to say that it was, of course. We can’t know one way or the oth­er on the basis of cur­rent­ly avail­able infor­ma­tion.

    Dr Anto­niou wrote a short let­ter to Nature Med­i­cine to point out these omis­sions in the authors’ case. Nature Med­i­cine has no method of sub­mit­ting a sim­ple let­ter to the edi­tor, so Dr Anto­niou had to sub­mit it as a Mat­ters Aris­ing com­men­tary, which the jour­nal defines as pre­sent­ing “chal­lenges or clar­i­fi­ca­tions” to an orig­i­nal pub­lished work.

    Dr Anto­niou’s com­ments were titled, “SARS-CoV­‑2 could have been cre­at­ed through lab­o­ra­to­ry manip­u­la­tion”. How­ev­er, Nature Med­i­cine refused to pub­lish them on the grounds that “we do not feel that they advance or clar­i­fy under­stand­ing” of the orig­i­nal arti­cle. The jour­nal offered no sci­en­tif­ic argu­ment to rebut his points.

    In our view, those points do offer clar­i­fi­ca­tion to the orig­i­nal arti­cle, and what’s more, there is a strong pub­lic inter­est case for mak­ing them pub­lic. That’s why we repro­duce Dr Antoniou’s let­ter below this arti­cle, with his per­mis­sion.

    Not genet­ic engi­neer­ing – but human inter­ven­tion

    There is, inci­den­tal­ly, anoth­er pos­si­ble way that SARS-CoV­‑2 could have been devel­oped in a lab­o­ra­to­ry, but in this case with­out using genet­ic engi­neer­ing. This was point­ed out by Niko­lai Petro­vsky, a researcher at the Col­lege of Med­i­cine and Pub­lic Health at Flinders Uni­ver­si­ty in South Aus­tralia. Petro­vsky says that coro­n­avirus­es can be cul­tured in lab dish­es with cells that have the human ACE2 recep­tor. Over time, the virus will gain adap­ta­tions that let it effi­cient­ly bind to those recep­tors. Along the way, that virus would pick up ran­dom genet­ic muta­tions that pop up but don’t do any­thing notice­able.

    “The result of these exper­i­ments is a virus that is high­ly vir­u­lent in humans but is suf­fi­cient­ly dif­fer­ent that it no longer resem­bles the orig­i­nal bat virus,” Petro­vsky said. “Because the muta­tions are acquired ran­dom­ly by selec­tion, there is no sig­na­ture of a human gene jock­ey, but this is clear­ly a virus still cre­at­ed by human inter­ven­tion.”

    Dr Anto­niou agrees that this method is pos­si­ble – but he points out that wait­ing for nature to pro­duce the desired muta­tions is a lot slow­er than using genet­ic engi­neer­ing to gen­er­ate a large num­ber of ran­dom muta­tions that you can then select for the desired out­come by a direct­ed iter­a­tive evo­lu­tion­ary pro­ce­dure.

    Because genet­ic engi­neer­ing great­ly speeds up the process, it is by far the most effi­cient way to gen­er­ate nov­el path­o­gen­ic virus­es in the lab.

    ...

    Con­clu­sion

    It is clear that there is no con­clu­sive evi­dence either way at this point as to whether SARS-CoV­‑2 arose by nat­ur­al muta­tion and selec­tion in ani­mal and/or human hosts or was genet­i­cal­ly engi­neered in a lab­o­ra­to­ry. And in this light, the ques­tion of where this virus came from should con­tin­ue to be explored with an open mind.

    *****

    SARS-CoV­‑2 could have been cre­at­ed through lab­o­ra­to­ry manip­u­la­tion

    Dr Michael Anto­niou

    Kris­t­ian Ander­sen and col­leagues (“The prox­i­mal ori­gin of SARS-CoV­‑2”, Nature Med­i­cine, 26: 450–452, 2020) argue that their amino acid sequence com­par­isons and com­pu­ta­tion­al mod­el­ling defin­i­tive­ly proves that SARS-CoV­‑2 has arisen through nat­ur­al muta­tion and selec­tion in ani­mal or human hosts, and not through lab­o­ra­to­ry manip­u­la­tion and acci­den­tal release. How­ev­er, although the authors may indeed be cor­rect in how they per­ceive SARS-CoV­‑2 to have arisen, the data they present does not exclude the pos­si­bil­i­ty that this new coro­n­avirus vari­ant could have been cre­at­ed through an in vit­ro, direct­ed iter­a­tive evo­lu­tion­ary selec­tion process (see https://en.wikipedia.org/wiki/Directed_evolution). Using this method, a very large library of ran­dom­ly muta­g­e­nized coro­n­avirus spike pro­teins could be select­ed for strong bind­ing to the ACE2 recep­tor and con­se­quent­ly high infec­tiv­i­ty of human cells. The pow­er of such direct­ed evo­lu­tion to select for opti­mal enzy­mat­ic and pro­tein-pro­tein inter­ac­tions was acknowl­edged by the award of the Nobel Prize in Chem­istry in 2018 (see https://www.nobelprize.org/prizes/chemistry/2018/summary/).

    ————-

    “Was the COVID-19 virus genet­i­cal­ly engi­neered?” by Claire Robin­son; GMWatch; 04/22/2020

    How­ev­er, the Lon­don-based mol­e­c­u­lar geneti­cist Dr Michael Anto­niou com­ment­ed that this line of rea­son­ing fails to take into account that there are a num­ber of lab­o­ra­to­ry-based sys­tems that can select for high affin­i­ty RBD vari­ants that are able to take into account the com­plex envi­ron­ment of a liv­ing organ­ism. This com­plex envi­ron­ment may impact the effi­cien­cy with which the SARS-CoV spike pro­tein can find the ACE2 recep­tor and bind to it. An RBD select­ed via these more real­is­tic real-world exper­i­men­tal sys­tems would be just as “ide­al”, or even more so, for human ACE2 bind­ing than any RBD that a com­put­er mod­el could pre­dict. And cru­cial­ly, it would like­ly be dif­fer­ent in amino acid sequence. So the fact that SARS-CoV­‑2 doesn’t have the same RBD amino acid sequence as the one that the com­put­er pro­gram pre­dict­ed in no way rules out the pos­si­bil­i­ty that it was genet­i­cal­ly engi­neered.”

    Yep, there’s absolute­ly no short­age of tech­niques that can devel­op an “opti­mized” viral fea­ture with­out sole­ly rely­ing on com­put­er sim­u­la­tions. Com­put­er sim­u­la­tions that aren’t event nec­es­sar­i­ly tru­ly opti­mized. We have no idea until the the­o­ret­i­cal sequences are test­ed. So if some­one uses one of the many tech­niques for ran­dom­ly gen­er­at­ing an opti­mized viral fea­ture using live ani­mals or cell cul­ture there should be no expec­ta­tion that what emerges from those exper­i­ments exact­ly match­es what’s pre­dict­ed by the sim­u­la­tions:

    ...
    Lim­its to com­put­er mod­el­ling

    Dr Anto­niou said that the authors’ rea­son­ing is not con­clu­sive because it is based large­ly on com­put­er mod­el­ling, which, he says, is “not defin­i­tive but only pre­dic­tive. It can­not tell us whether any giv­en virus would be opti­mized for infec­tiv­i­ty in a real world sce­nario, such as in the human body. That’s because the envi­ron­ment of the human body will influ­ence how the virus inter­acts with the recep­tor. You can’t mod­el that accu­rate­ly with com­put­er mod­el­ling as there are sim­ply too many vari­ables to fac­tor into the equa­tion.”

    Dr Anto­niou added, “Peo­ple can put too much faith in com­put­er pro­grams, but they are only a begin­ning. You then have to prove whether the com­put­er program’s pre­dic­tion is cor­rect or not by direct exper­i­men­ta­tion in a liv­ing organ­ism. This has not been done in the case of this hypoth­e­sis, so it remains unproven.”

    It is even pos­si­ble that SARS-CoV­‑2 was opti­mized using a liv­ing organ­ism mod­el, result­ing in a virus that is bet­ter at infect­ing humans than any com­put­er mod­el could pre­dict.

    ...

    And one of those tech­niques for devel­op­ing opti­mized (or, if not opti­mized at least improved) viral fea­tures, direct­ed iter­a­tive evo­lu­tion­ary selec­tion process, won the Nobel Prize in Chem­istry in 2018. It’s a tech­nique that can work with human cell cul­tures. You don’t need a bunch of live humans to con­duct these exper­i­ments. You just need a bunch of human cells:

    ...
    But Dr Anto­niou told us that while the authors did indeed show that SARS-CoV­‑2 was unlike­ly to have been built by delib­er­ate genet­ic engi­neer­ing from a pre­vi­ous­ly used virus back­bone, that’s not the only way of con­struct­ing a virus. There is anoth­er method by which an enhanced-infec­tiv­i­ty virus can be engi­neered in the lab.

    A well-known alter­na­tive

    A well-known alter­na­tive process that could have been used has the cum­ber­some name of “direct­ed iter­a­tive evo­lu­tion­ary selec­tion process”. In this case, it would involve using genet­ic engi­neer­ing to gen­er­ate a large num­ber of ran­dom­ly mutat­ed ver­sions of the SARS-CoV spike pro­tein recep­tor bind­ing domain (RBD), which would then be select­ed for strong bind­ing to the ACE2 recep­tor and con­se­quent­ly high infec­tiv­i­ty of human cells.

    This selec­tion can be done either with puri­fied pro­teins or, bet­ter still, with a mix­ture of whole coro­n­avirus (CoV) prepa­ra­tions and human cells in tis­sue cul­ture. Alter­na­tive­ly, the SARS-CoV spike pro­tein vari­ants can be genet­i­cal­ly engi­neered with­in what is known as a “phage dis­play library”. A phage is a virus that infects bac­te­ria and can be genet­i­cal­ly engi­neered to express on its exte­ri­or coat the CoV spike pro­tein with a large num­ber of vari­ants of the RBD. This prepa­ra­tion of phage, dis­play­ing on its sur­face a “library” of CoV spike pro­tein vari­ants, is then added to human cells under lab­o­ra­to­ry cul­ture con­di­tions in order to select for those that bind to the ACE2 recep­tor.

    ...

    Such a direct­ed iter­a­tive evo­lu­tion­ary selec­tion process is a fre­quent­ly used method in lab­o­ra­to­ry research. So there is lit­tle or no pos­si­bil­i­ty that the Nature Med­i­cine arti­cle authors haven’t heard of it – not least, as it is con­sid­ered so sci­en­tif­i­cal­ly impor­tant that its inven­tors were award­ed the Nobel Prize in Chem­istry in 2018.
    ...

    There’s are even slow­er, undi­rect­ed tech­niques for ran­dom­ly allow­ing evo­lu­tion in cell cul­tures to come up with pre­vi­ous­ly unknown viral fea­tures. As Niko­lai Petro­vsky, a researcher at the Col­lege of Med­i­cine and Pub­lic Health at Flinders Uni­ver­si­ty in South Aus­tralia, recent­ly point­ed out, just let­ting coro­n­avirus­es prop­a­gate in human cell cul­tures would even­tu­al­ly come up with new virus­es that no longer resem­ble the orig­i­nal virus. It might take a long time for the desired end result, but because “there is no sig­na­ture of a human gene jock­ey, but this is clear­ly a virus still cre­at­ed by human inter­ven­tion”:

    ...
    Not genet­ic engi­neer­ing – but human inter­ven­tion

    There is, inci­den­tal­ly, anoth­er pos­si­ble way that SARS-CoV­‑2 could have been devel­oped in a lab­o­ra­to­ry, but in this case with­out using genet­ic engi­neer­ing. This was point­ed out by Niko­lai Petro­vsky, a researcher at the Col­lege of Med­i­cine and Pub­lic Health at Flinders Uni­ver­si­ty in South Aus­tralia. Petro­vsky says that coro­n­avirus­es can be cul­tured in lab dish­es with cells that have the human ACE2 recep­tor. Over time, the virus will gain adap­ta­tions that let it effi­cient­ly bind to those recep­tors. Along the way, that virus would pick up ran­dom genet­ic muta­tions that pop up but don’t do any­thing notice­able.

    “The result of these exper­i­ments is a virus that is high­ly vir­u­lent in humans but is suf­fi­cient­ly dif­fer­ent that it no longer resem­bles the orig­i­nal bat virus,” Petro­vsky said. “Because the muta­tions are acquired ran­dom­ly by selec­tion, there is no sig­na­ture of a human gene jock­ey, but this is clear­ly a virus still cre­at­ed by human inter­ven­tion.”

    Dr Anto­niou agrees that this method is pos­si­ble – but he points out that wait­ing for nature to pro­duce the desired muta­tions is a lot slow­er than using genet­ic engi­neer­ing to gen­er­ate a large num­ber of ran­dom muta­tions that you can then select for the desired out­come by a direct­ed iter­a­tive evo­lu­tion­ary pro­ce­dure.
    ...

    And yet, for what­ev­er rea­son, when Dr Anto­niou attempt­ed to point this out in his let­ter to Nature Med­i­cine he was reject­ed due to not adding any clar­i­ty to the sit­u­a­tion. Why exact­ly bring­ing up these valid cri­tiques don’t add clar­i­ty remains unclear. We’ll see if the cri­tiques by sci­en­tists like New­man and Anto­niou are ever giv­en their prop­er air­ing. But since they are cri­tiques that are root­ed in the recog­ni­tion that it’s unfor­tu­nate­ly shock­ing­ly easy to cre­ate nov­el virus­es with pre­vi­ous­ly unknown ‘opti­mized’ fea­tures we can trag­i­cal­ly be pret­ty con­fi­dent that SARS-CoV­‑2 won’t be the last nov­el mys­tery virus of this ‘nature’. Hope­ful­ly future crit­ics have a more recep­tive audience...a more recep­tive audi­ence that has­n’t already been wiped out by a fas­cist dooms­day virus.

    Posted by Pterrafractyl | May 2, 2020, 3:57 pm
  4. @Pterrafractyl–

    Good work! Some­thing to be borne in mind when assess­ing New­man’s and Anto­niou’s cri­tique is that dev­as­tat­ing­ly impor­tant Whit­ney Webb arti­cle:

    https://spitfirelist.com/news/disturbing-article-about-darpa-and-bat-borne-coronaviruses/

    DARPA has state-of-the-art super com­put­ers, twined with Arti­fi­cial Intel­li­gence.

    When applied to the sce­nar­ios described by New­man and Antonon­iou, it would be VERY easy to devise such organ­isms.

    And they were DEFINITELY study­ing bat-borne coro­n­avirus­es.

    Best,

    Dave

    Posted by Dave Emory | May 3, 2020, 4:09 pm
  5. Oh look: a rule change to fed­er­al nurs­ing home infec­tion con­trol reg­u­la­tions that the Trump admin­is­tra­tion pro­posed last year — before the COVID-19 out­break — is still under con­sid­er­a­tion. The pro­posed change hap­pens to gut the fed­er­al reg­u­la­tions for infec­tion con­trol, of course. So the Trump admin­is­tra­tion is active­ly con­sid­er­ing the gut­ting of fed­er­al nurs­ing home infec­tion con­trol reg­u­la­tions. In the mid­dle of a viral pan­dem­ic dis­tin­guished by it hyper-infec­tious­ness. Yep.

    The rule change was pro­posed by the Cen­ters for Medicare and Med­ic­aid Ser­vices (CMS), a ‘usu­al sus­pect’ agency for the Trump admin­is­tra­tion’s attacks on the safe­ty-net. The pro­pos­al would change the amount of time an infec­tion pre­ven­tion­ist must devote to a nurs­ing home. Cur­rent­ly, an infec­tion pre­ven­tion­ist has to be work­ing at least part-time at a home. The new rule would be for the pre­ven­tion­ist spend to “suf­fi­cient time” at the facil­i­ty, which is an unde­fined term that lets the nurs­ing home decide how much time should be spent. So if a nurs­ing home decides that it does­n’t need to ded­i­cate as mon­ey resources to infec­tion pre­ven­tion as the cur­rent rules man­date that will be up to them.

    The rule change does­n’t require con­gres­sion­al approval so CMS can uni­lat­er­al­ly make this change on its own. And while the change has­n’t been final­ized yet, CMS defend­ed the rule again just last week. So the CMS pro­posed a rule change last year that would have been dan­ger­ous to seniors even with­out a glob­al hyper-infec­tious pan­dem­ic, then a his­tor­i­cal­ly hyper-infec­tious pan­dem­ic that hits the elder­ly the hard­est breaks out and CMS is stick­ing with its rule change. So in case it was­n’t already abun­dant­ly clear from the all of the pri­or moves to restrict Medicare and Med­ic­aid cov­er­age that Trump’s CMS is look­ing for excus­es to kill off the vul­ner­a­ble here’s your lat­est exam­ple:

    USA TODAY

    ‘It makes no sense’: Feds con­sid­er relax­ing infec­tion con­trol in US nurs­ing homes

    Marisa Kwiatkows­ki and Tri­cia L. Nadol­ny
    Pub­lished 6:00 a.m. ET May 4, 2020 | Updat­ed 9:36 a.m. ET May 5, 2020

    The fed­er­al gov­ern­ment is con­sid­er­ing rolling back infec­tion con­trol require­ments in U.S. nurs­ing homes – even as the long-term-care indus­try’s res­i­dents and work­ers are over­whelmed by the coro­n­avirus.

    A rule pro­posed last year by the Cen­ters for Medicare and Med­ic­aid Ser­vices (CMS) would mod­i­fy the amount of time an infec­tion pre­ven­tion­ist must devote to a facil­i­ty from at least part-time to “suf­fi­cient time,” an unde­fined term that lets the facil­i­ty decide how much time should be spent. The reg­u­la­tion has not been final­ized, but CMS last week defend­ed its pro­pos­al, say­ing it aims to reduce reg­u­la­to­ry bur­den and strength­en infec­tion con­trol.

    Oppo­nents of the change said the rule could leave nurs­ing home res­i­dents more vul­ner­a­ble to infec­tion. They expressed con­cern, espe­cial­ly giv­en the dev­as­ta­tion COVID-19 has caused with­in long-term care facil­i­ties.

    It makes no sense at all – pri­or to pan­dem­ic, but more so now dur­ing a pan­dem­ic – to roll back any of the nec­es­sary infec­tion and con­trol require­ments and the fed­er­al reg­u­la­tions,” said Lind­say Heck­ler, a super­vis­ing attor­ney at the Cen­ter for Elder Law & Jus­tice, a civ­il legal ser­vices agency in Buf­fa­lo, New York. “They should be strength­en­ing these infec­tion and con­trol require­ments.”

    CMS has acknowl­edged that infec­tion is “the lead­ing cause of mor­bid­i­ty and mor­tal­i­ty” in the nation’s 15,600 nurs­ing homes. In its pro­posed rule, the agency said 1.6 mil­lion to 3.8 mil­lion infec­tions occur each year in those facil­i­ties, with almost 388,000 deaths attrib­uted to infec­tions.

    The coro­n­avirus has put a spot­light on the prob­lem. More than 16,000 long-term-care res­i­dents and staff have died of COVID-19, accord­ing to a USA TODAY analy­sis of gov­ern­ment data. And near­ly 97,000 res­i­dents and staff have test­ed pos­i­tive for the virus. Those fig­ures are an under­count, because test­ing has been lim­it­ed and many states have not released full data.

    CMS told USA TODAY its rule would allow facil­i­ties to deter­mine for them­selves the time need­ed for infec­tion pre­ven­tion and go above part-time when war­rant­ed.

    “This is a per­son-cen­tered approach to care and would allow CMS to hold facil­i­ties account­able by hav­ing the infec­tion pre­ven­tion­ist onsite full time, espe­cial­ly in times of an out­break,” the agency said in a state­ment last week.

    The changes were first pro­posed in July 2019, part of an ongo­ing effort by the Trump admin­is­tra­tion to reduce reg­u­la­tions for nurs­ing home providers and sup­pli­ers. In addi­tion to mod­i­fy­ing the infec­tion pre­ven­tion­ist require­ment, the pro­posed rule would also reduce the need for a facil­i­ty-wide assess­ment from once a year to every oth­er year and allow cer­tain facil­i­ties to dis­re­gard a require­ment that caps res­i­dents at two per room. CMS said the changes would reform “unnec­es­sary, obso­lete or exces­sive­ly bur­den­some” require­ments.

    CMS, which has the author­i­ty to change reg­u­la­tions on nurs­ing homes with­out leg­is­la­tion, said the pro­pos­al is still under review. There were 1,731 com­ments on the rule – from nurs­ing home own­ers to advo­cates to res­i­dents and their fam­i­ly mem­bers – when the peri­od for pub­lic input closed in Sep­tem­ber.

    Some of the sub­mis­sions are pre­scient giv­en what has since occurred with COVID-19.

    “Too many peo­ple have died and too many have suf­fered,” Alice Hedt, a for­mer direc­tor of the Nation­al Ombuds­man Cen­ter, wrote in a com­ment post­ed Sept. 24. “Min­i­miz­ing the require­ments of the Infec­tion Pre­ven­tion­ist when we know infec­tions can be pre­vent­ed and addressed will result in even more deaths and suf­fer­ing. I per­son­al­ly think this per­son should be full time in every facil­i­ty until the death rate from infec­tion and unnec­es­sary hos­pi­tal­iza­tions decline by fifty per­cent.”

    Hedt, who spent 30 years as an advo­cate for long-term care res­i­dents, called the pro­pos­al “a slap in the face of res­i­dents who are more frail than any­time in our long term care his­to­ry.”

    Experts say COVID-19’s dev­as­tat­ing effect on peo­ple in long-term care is the result of a com­plex mix of fac­tors, includ­ing the char­ac­ter­is­tics of the virus, vul­ner­a­bil­i­ty of old­er adults and those with under­ly­ing con­di­tions, staffing lev­els and nation­al avail­abil­i­ty of test­ing and per­son­al pro­tec­tive equip­ment. For some, the virus’ effect on nurs­ing homes has renewed their con­cerns about the pro­posed rule.

    “That soft­en­ing of that rule I think, in ret­ro­spect, is exact­ly the wrong thing,” said Christo­pher Lax­ton, exec­u­tive direc­tor of the Soci­ety for Post-Acute and Long-Term Care Med­i­cine.

    Lax­ton, whose asso­ci­a­tion rep­re­sents about 5,500 med­ical pro­fes­sion­als work­ing in long-term-care set­tings, last year offered tepid sup­port of the change, writ­ing that his group didn’t object to the new lan­guage but that both terms “may be con­fus­ing and dif­fi­cult to define.” He wrote that the amount of time spent on infec­tion pre­ven­tion should be based on real-life fac­tors, such as the facility’s risk assess­ment, sea­son­al changes and the pres­ence of out­breaks.

    In an inter­view last week, he said it is “a dif­fer­ent world than when we first com­ment­ed on that pro­pos­al.”

    “At this point, suf­fi­cient time for an infec­tion con­trol pre­ven­tion­ist in a build­ing means full time,” he said. “And it means ded­i­cat­ed to a sin­gle build­ing. And being there every day. That’s what suf­fi­cient means in this con­text. It may not mean that out­side of a COVID pan­dem­ic. But it cer­tain­ly means it now.”

    ‘Some­times reg­u­la­tion hin­ders us’

    With­in the long-term-care indus­try, some are less con­vinced that leav­ing the rule as is, or even strength­en­ing it, would make a mean­ing­ful dif­fer­ence in infec­tion con­trol.

    “Some­times reg­u­la­tion hin­ders us from putting resources where we know they need to be,” said Dr. Gre­go­ry John­son, chief med­ical offi­cer of the Evan­gel­i­cal Luther­an Good Samar­i­tan Soci­ety, the largest not-for-prof­it provider of long-term care and senior ser­vices in the Unit­ed States.

    He not­ed that only a small por­tion of the facil­i­ty-wide assess­ment – which the pro­posed reg­u­la­tions would require to be con­duct­ed every oth­er year rather than annu­al­ly – focus­es on infec­tion con­trol. The amount of work that goes into what can become a 300-page doc­u­ment is “colos­sal,” John­son said, and there are oth­er reg­u­la­tions that address infec­tion con­trol.

    Dur­ing the pan­dem­ic, he said, his orga­ni­za­tion has “far exceed­ed” even the part-time require­ment. John­son said they began imple­ment­ing vis­i­tor restric­tions and oth­er pre­ven­ta­tive mea­sures in ear­ly March. As of Sun­day, the Good Samar­i­tan Soci­ety said 26 of its 143 skilled nurs­ing facil­i­ties had at least one con­firmed case of COVID-19.

    John­son said the orga­ni­za­tion – which oper­ates in 26 states – grap­ples with dif­fer­ing local, state and fed­er­al reg­u­la­tions and tries to sur­pass them.

    Too often, John­son said, the pub­lic hears only about the nurs­ing homes that are “bad apples.”

    “There are a whole lot of peo­ple out there in this busi­ness who are doing it because of a deep care and a deep com­mit­ment to mis­sion,” he said.

    Com­bined, the CMS reg­u­la­tions serve as the basis for fed­er­al inspec­tions that are con­duct­ed in U.S. nurs­ing homes. Mark Parkin­son, pres­i­dent and CEO of the Amer­i­can Health Care Asso­ci­a­tion and Nation­al Cen­ter for Assist­ed Liv­ing, said that sur­vey process is “bro­ken on many lev­els” because it mea­sures too many things and is too puni­tive.

    His orga­ni­za­tion, which rep­re­sents more than 14,000 long-term-care facil­i­ties that col­lec­tive­ly pro­vide care to more than 5 mil­lion peo­ple, said it sup­ports qual­i­ty infec­tion pre­ven­tion in facil­i­ties but is behind CMS’ pro­posed rule change. The orga­ni­za­tion said in a state­ment that “more over­sight is not the answer to what has hap­pened dur­ing the pan­dem­ic – it would reduce crit­i­cal resources these cen­ters need, or even put them at risk of clos­ing.” But it also said facil­i­ties can always do more.

    “When we get through this, the entire coun­try will need to have a seri­ous dis­cus­sion and reck­on­ing about our infec­tion con­trol prac­tices in health care set­tings and through­out soci­ety,” the state­ment said.

    Oppo­si­tion to pro­posed rule

    Peo­ple who oppose CMS’ rule change say COVID-19 has proven that strong infec­tion con­trol is para­mount.

    The Asso­ci­a­tion for Pro­fes­sion­als in Infec­tion Con­trol and Epi­demi­ol­o­gy (APIC) has remained stead­fast in its oppo­si­tion to CMS’ pro­posed rule. The non­prof­it orga­ni­za­tion said it was dis­ap­point­ed to see CMS acqui­esce to the argu­ment that com­pli­ance is over­ly bur­den­some and expressed con­cern that the fed­er­al gov­ern­ment was try­ing to change the reg­u­la­tions, which have been phased in since late 2016, before their impact has ful­ly been felt.

    “The COIVD-19 out­break has real­ly brought to light the oppor­tu­ni­ties and vul­ner­a­bil­i­ties of long-term care and the need for effec­tive infec­tion pre­ven­tion,” said APIC Pres­i­dent Con­nie Steed, who is the direc­tor of infec­tion pre­ven­tion and con­trol at Pris­ma Health in South Car­oli­na. “And it does­n’t mat­ter if it’s COVID-19 or influen­za or oth­er con­cern­ing infec­tions and out­breaks that can occur in these set­tings. A robust infec­tion pre­ven­tion con­trol pro­gram is real­ly imper­a­tive for these types of facil­i­ties.”

    Car­ol Buck­n­er, a reg­is­tered nurse who works in tele­health, said she has long had con­cerns about the qual­i­ty of care at the nurs­ing home in Rochester, New York, where her broth­er lives, The Pearl Nurs­ing and Reha­bil­i­ta­tion. The cen­ter, which until recent­ly was named New Roc Nurs­ing and Reha­bil­i­ta­tion Cen­ter, is one of 88 nurs­ing homes iden­ti­fied by CMS as a Spe­cial Focus Facil­i­ty, homes that have chron­ic defi­cien­cies and face addi­tion­al gov­ern­ment over­sight.

    “There’s not enough staff. They’re not trained. And there’s no direct over­sight. I nev­er see a nurse in there unless they’re pass­ing meds,” she said. “And then you add COVID into this?”

    The facil­i­ty’s admin­is­tra­tor did not respond to a request for com­ment

    ...

    ———–

    “ ‘It makes no sense’: Feds con­sid­er relax­ing infec­tion con­trol in US nurs­ing homes” by Marisa Kwiatkows­ki and Tri­cia L. Nadol­ny; USA TODAY; 05/04/2020

    “A rule pro­posed last year by the Cen­ters for Medicare and Med­ic­aid Ser­vices (CMS) would mod­i­fy the amount of time an infec­tion pre­ven­tion­ist must devote to a facil­i­ty from at least part-time to “suf­fi­cient time,” an unde­fined term that lets the facil­i­ty decide how much time should be spent. The reg­u­la­tion has not been final­ized, but CMS last week defend­ed its pro­pos­al, say­ing it aims to reduce reg­u­la­to­ry bur­den and strength­en infec­tion con­trol.

    CMS dou­bled-down just last week. That sure sounds like the agency is seri­ous­ly intent on mak­ing that rule change. So now each nurs­ing home oper­a­tor will get to decide for itself how much an infec­tion pre­ven­tion­ists needs to spend at the home. “Part-time” is no longer the min­i­mum:

    ...
    CMS has acknowl­edged that infec­tion is “the lead­ing cause of mor­bid­i­ty and mor­tal­i­ty” in the nation’s 15,600 nurs­ing homes. In its pro­posed rule, the agency said 1.6 mil­lion to 3.8 mil­lion infec­tions occur each year in those facil­i­ties, with almost 388,000 deaths attrib­uted to infec­tions.

    The coro­n­avirus has put a spot­light on the prob­lem. More than 16,000 long-term-care res­i­dents and staff have died of COVID-19, accord­ing to a USA TODAY analy­sis of gov­ern­ment data. And near­ly 97,000 res­i­dents and staff have test­ed pos­i­tive for the virus. Those fig­ures are an under­count, because test­ing has been lim­it­ed and many states have not released full data.

    CMS told USA TODAY its rule would allow facil­i­ties to deter­mine for them­selves the time need­ed for infec­tion pre­ven­tion and go above part-time when war­rant­ed.

    “This is a per­son-cen­tered approach to care and would allow CMS to hold facil­i­ties account­able by hav­ing the infec­tion pre­ven­tion­ist onsite full time, espe­cial­ly in times of an out­break,” the agency said in a state­ment last week.

    The changes were first pro­posed in July 2019, part of an ongo­ing effort by the Trump admin­is­tra­tion to reduce reg­u­la­tions for nurs­ing home providers and sup­pli­ers. In addi­tion to mod­i­fy­ing the infec­tion pre­ven­tion­ist require­ment, the pro­posed rule would also reduce the need for a facil­i­ty-wide assess­ment from once a year to every oth­er year and allow cer­tain facil­i­ties to dis­re­gard a require­ment that caps res­i­dents at two per room. CMS said the changes would reform “unnec­es­sary, obso­lete or exces­sive­ly bur­den­some” require­ments.

    CMS, which has the author­i­ty to change reg­u­la­tions on nurs­ing homes with­out leg­is­la­tion, said the pro­pos­al is still under review. There were 1,731 com­ments on the rule – from nurs­ing home own­ers to advo­cates to res­i­dents and their fam­i­ly mem­bers – when the peri­od for pub­lic input closed in Sep­tem­ber.

    ...

    The Asso­ci­a­tion for Pro­fes­sion­als in Infec­tion Con­trol and Epi­demi­ol­o­gy (APIC) has remained stead­fast in its oppo­si­tion to CMS’ pro­posed rule. The non­prof­it orga­ni­za­tion said it was dis­ap­point­ed to see CMS acqui­esce to the argu­ment that com­pli­ance is over­ly bur­den­some and expressed con­cern that the fed­er­al gov­ern­ment was try­ing to change the reg­u­la­tions, which have been phased in since late 2016, before their impact has ful­ly been felt.
    ...

    And note the omi­nous warn­ing from indus­try lob­by­ist who is back­ing this rule change: The Amer­i­can Health Care Asso­ci­a­tion and Nation­al Cen­ter for Assist­ed Liv­ing, which rep­re­sents 14,000 long-term-care facil­i­ties, warns that if more infec­tion con­trol over­sight is imposed dur­ing this pan­dem­ic it might put nurs­ing homes at risk of clos­ing. Think about that state­ment. The indus­try lob­by­ing group is basi­cal­ly say­ing that the cost of increas­ing infec­tion con­trols dur­ing this pan­dem­ic might be too much for nurs­ing homes to finan­cial han­dle. In oth­er words, many nurs­ing home oper­a­tors are based on a busi­ness mod­el that pre­cludes effec­tive infec­tion con­trol. That’s effec­tive­ly what this indus­try lob­by­ing group has admit­ted which sure sounds like a pow­er­ful rea­son to increase over­sight of the indus­try:

    ...
    Com­bined, the CMS reg­u­la­tions serve as the basis for fed­er­al inspec­tions that are con­duct­ed in U.S. nurs­ing homes. Mark Parkin­son, pres­i­dent and CEO of the Amer­i­can Health Care Asso­ci­a­tion and Nation­al Cen­ter for Assist­ed Liv­ing, said that sur­vey process is “bro­ken on many lev­els” because it mea­sures too many things and is too puni­tive.

    His orga­ni­za­tion, which rep­re­sents more than 14,000 long-term-care facil­i­ties that col­lec­tive­ly pro­vide care to more than 5 mil­lion peo­ple, said it sup­ports qual­i­ty infec­tion pre­ven­tion in facil­i­ties but is behind CMS’ pro­posed rule change. The orga­ni­za­tion said in a state­ment that “more over­sight is not the answer to what has hap­pened dur­ing the pan­dem­ic – it would reduce crit­i­cal resources these cen­ters need, or even put them at risk of clos­ing.” But it also said facil­i­ties can always do more.

    When we get through this, the entire coun­try will need to have a seri­ous dis­cus­sion and reck­on­ing about our infec­tion con­trol prac­tices in health care set­tings and through­out soci­ety,” the state­ment said.
    ...

    As the lob­by­ing group sug­gests, when we get through this, the entire US will no doubt need to have a seri­ous dis­cus­sion and reck­on­ing about its infec­tion con­trol prac­tices in health care set­tings and through­out soci­ety. A reck­on­ing that should prob­a­bly take place before we get through this and belat­ed­ly dis­cov­ery that large num­bers of nurs­ing home deaths could have been pre­vent­ed with more rig­or­ous infec­tion con­trols.

    So as we can see, Trump’s CMS is tak­ing indeed steps to deal with the pan­dem­ic. Specif­i­cal­ly, steps to ensure car­nage in nurs­ing homes across the US but espe­cial­ly the nurs­ing homes oper­at­ing on the tight­est bud­gets. That’s where we should expect max­i­mal car­nage. As the indus­try lob­by is open­ly warn­ing us, some nurs­ing homes sim­ply aren’t going to be able to stay open if they need to deal with the costs of “more over­sight”. Are the nurs­ing homes that can’t deal with the costs of “more over­sight” going to able and will­ing to deal with the costs of greater infec­tion con­trols on their own after that over­sight is lift­ed? We’ll find out. Pre­sum­ably in the form of even more nurs­ing home mass deaths.

    In oth­er news, the state of Con­necti­cut just released a new report on the COVID deaths in the state in the last week of April. Guess where 90 per­cent of the deaths took place:

    Hart­ford Courant

    Near­ly 90 per­cent of the coro­n­avirus deaths in Con­necti­cut last week were nurs­ing home patients

    By Dave Alti­mari
    May 06, 2020

    Near­ly 90% of the COVID-relat­ed deaths record­ed by the state last week occurred in nurs­ing homes as COVID-19 con­tin­ues to attack res­i­dents of long-term care facil­i­ties and the state pre­pares to par­tial­ly reopen lat­er this month.

    Between April 22 and April 29, the state’s death total rose from 1,544 to 2,089, or 545 new deaths, accord­ing to data released by the state Depart­ment of Pub­lic Health. In that same sev­en-day peri­od nurs­ing home deaths rose from 768 to 1,249, mean­ing 481 among the 545 new deaths — about 88% — were nurs­ing home patients.

    “This brings tears to everyone’s eyes,” said Yale epi­demi­ol­o­gist Dr. Albert Ko, who also is co-chair­man of Gov. Ned Lamont’s advi­so­ry board to reopen the state.

    Ko said the nurs­ing home pop­u­la­tion is like “princess dia­monds” that need to be pro­tect­ed. He said the advi­so­ry board has talked about the ris­ing nurs­ing home deaths but is not ready to reveal any rec­om­men­da­tions it may have.

    “We’re real­ly wor­ried about this group and one of the major things we need to do is pro­tect them,” Ko said. “But this virus blows up like wild­fire in the facil­i­ties and is hard to con­tain.”

    Con­necti­cut is not alone in suf­fer­ing a high rate of deaths in its nurs­ing homes. Mass­a­chu­setts, New Jer­sey and Rhode Island have also seen sim­i­lar increas­es and on Tues­day New York announced that there had been about 1,700 more deaths in nurs­ing homes than had been pre­vi­ous­ly report­ed.

    Over­all about 60% of Connecticut’s COVID-19 deaths have been nurs­ing home patients — sim­i­lar num­bers to Mass­a­chu­setts and New Jer­sey. In Rhode Island the death rate is near­ly 70%.

    DPH spokesman Av Har­ris said the depart­ment is about to ramp up its test­ing pro­gram as sup­plies have start­ed to arrive and are shipped to nurs­ing homes across the state. It will be a large task, as there are more than 20,000 elder­ly res­i­dents in the state’s 215 nurs­ing homes.

    “As far as test­ing for nurs­ing home res­i­dents, DPH has dis­trib­uted hun­dreds of new test­ing kits to nurs­ing homes in Con­necti­cut this week and we expect the capac­i­ty for test­ing of the res­i­dents most vul­ner­a­ble to COVID-19 to great­ly expand in the com­ing weeks,” Har­ris said.

    At a press con­fer­ence Thurs­day Gov. Lam­ont said while hos­pi­tal­iza­tions had gone down for the eighth straight day there were still 89 deaths and the nurs­ing home deaths were “some­thing we have to think about seri­ous­ly.”

    Last week a team from the Con­necti­cut Nation­al Guard arrived to assist DPH offi­cials in inspect­ing all 215 nurs­ing homes in the state to ensure they are fol­low­ing prop­er infec­tion con­trol pro­ce­dures, have ample staff and enough PPE for them to wear while car­ing for COVID-19 patients.

    DPH also asked for assis­tance from the fed­er­al Cen­ters for Dis­ease Con­trol.

    “The Cen­ters for Dis­ease Con­trol and Pre­ven­tion has accom­pa­nied DPH staff on more than 47 dif­fer­ent nurs­ing home sur­veys and pro­vid­ed con­sul­ta­tion to sur­vey­ors and the nurs­ing homes rel­a­tive to infec­tion con­trol and pre­ven­tion,” Har­ris said.

    “We are com­mit­ted to doing every­thing pos­si­ble to slow down the spread of this virus in our long-term care facil­i­ties and save as many lives as we can,” Har­ris said.

    Test­ing health care work­ers will be impor­tant as the state reopens, accord­ing to Dr. Sum­mer McGee, dean of the Uni­ver­si­ty of New Haven’s School of Health Sci­ences.

    “While nurs­ing home cas­es are some­what iso­lat­ed, we still need to remain vig­i­lant to ensure health care work­ers in those facil­i­ties are not result­ing in com­mu­ni­ty spread and that strict vis­i­ta­tion restric­tions con­tin­ue to lim­it the spread out­side of nurs­ing homes,” McGee said. “Nurs­ing home res­i­dents are a large per­cent­age of the deaths in Con­necti­cut but they are not the only source of new cas­es. New case counts demon­strate that com­mu­ni­ty spread is still tak­ing place.”

    Over­all, Ko said that death rates are nor­mal­ly a few weeks behind oth­er fac­tors that experts look at in deter­min­ing the path of a virus.

    “In Con­necti­cut we clear­ly have decreas­ing trans­mis­sion rates and we are com­ing down the curve,” Ko said.

    Ko said nurs­ing home deaths are slight­ly dif­fer­ent than peo­ple who die in the com­mu­ni­ty in terms of trans­mit­ting the virus, since they are most­ly in con­fined areas and not out in the pub­lic spread­ing the dis­ease.

    ...

    ———–

    “Near­ly 90 per­cent of the coro­n­avirus deaths in Con­necti­cut last week were nurs­ing home patients” by Dave Alti­mari; Hart­ford Courant; 05/06/2020

    Between April 22 and April 29, the state’s death total rose from 1,544 to 2,089, or 545 new deaths, accord­ing to data released by the state Depart­ment of Pub­lic Health. In that same sev­en-day peri­od nurs­ing home deaths rose from 768 to 1,249, mean­ing 481 among the 545 new deaths — about 88% — were nurs­ing home patients.”

    So Con­necti­cut’s death count rose by around 1/3rd in the last week of April and 88% of those new deaths were in nurs­ing homes. Keep in mind that this would be the same week the CMS dou­bled-down on is pro­posed relax­ation of the infec­tion con­trol rule change.

    And it’s not just Con­necti­cut that’s find­ing the bulk of new deaths in nurs­ing homes. That’s been the case across the North East US:

    ...
    Con­necti­cut is not alone in suf­fer­ing a high rate of deaths in its nurs­ing homes. Mass­a­chu­setts, New Jer­sey and Rhode Island have also seen sim­i­lar increas­es and on Tues­day New York announced that there had been about 1,700 more deaths in nurs­ing homes than had been pre­vi­ous­ly report­ed.

    Over­all about 60% of Connecticut’s COVID-19 deaths have been nurs­ing home patients — sim­i­lar num­bers to Mass­a­chu­setts and New Jer­sey. In Rhode Island the death rate is near­ly 70%.
    ...

    And note what Con­necti­cut doing in response to this nurs­ing home pan­dem­ic: call­ing in the Con­necti­cut Nation­al Guard and fed­er­al CDC to help state pub­lic health offi­cial inspect all of the states 215 nurs­ing homes to ensure the are fol­low­ing prop­er infec­tion con­trol pro­ce­dures:

    ...
    Last week a team from the Con­necti­cut Nation­al Guard arrived to assist DPH offi­cials in inspect­ing all 215 nurs­ing homes in the state to ensure they are fol­low­ing prop­er infec­tion con­trol pro­ce­dures, have ample staff and enough PPE for them to wear while car­ing for COVID-19 patients.

    DPH also asked for assis­tance from the fed­er­al Cen­ters for Dis­ease Con­trol.

    “The Cen­ters for Dis­ease Con­trol and Pre­ven­tion has accom­pa­nied DPH staff on more than 47 dif­fer­ent nurs­ing home sur­veys and pro­vid­ed con­sul­ta­tion to sur­vey­ors and the nurs­ing homes rel­a­tive to infec­tion con­trol and pre­ven­tion,” Har­ris said.
    ...

    So that gives us a glimpse of how states are prob­a­bly going to be deal­ing with grow­ing nurs­ing home pan­dem­ic after the CMS relax­es that rule and the pan­dem­ic gets even worse: call in the nation­al guard and CDC to con­duct those infec­tion con­trol inspec­tions instead.

    In relat­ed news, Pres­i­dent Trump’s poll num­bers appear to be suf­fer­ing with senior vot­ers, a core part of his vot­ing base, in response to his han­dling of the coro­n­avirus pan­dem­ic. Image that.

    Posted by Pterrafractyl | May 6, 2020, 12:58 pm
  6. Here’s a set of arti­cles about a deci­sion by the US mil­i­tary that we real­ly have to hope is root­ed in an abun­dance of cau­tion and not an abun­dance of evi­dence. Because if there’s an abun­dance of evi­dence behind this deci­sion by the mil­i­tary that’s real­ly bad news for more than just the mil­i­tary:

    A Depart­ment of Defense memo just pub­lished by the Mil­i­tary Times indi­cates that new US mil­i­tary recruits are going to be screen for COVID-19 cas­es and if they have a his­to­ry of COVID-19 they will be per­ma­nent­ly banned from mil­i­tary ser­vice:

    Mil­i­tary Times

    Coro­n­avirus sur­vivors banned from join­ing the mil­i­tary

    Meghann Myers
    05/06/2020

    As the Defense Depart­ment nego­ti­ates its way through the coro­n­avirus pan­dem­ic and its fall­out, mil­i­tary entrance pro­cess­ing sta­tions are work­ing with new guid­ance when it comes to bring­ing COVID-19 sur­vivors into the ser­vices.

    A past COVID-19 diag­no­sis is a no-go for pro­cess­ing, accord­ing to a recent­ly released MEPCOM memo cir­cu­lat­ing on Twit­ter.

    “Dur­ing the med­ical his­to­ry inter­view or exam­i­na­tion, a his­to­ry of COVID-19, con­firmed by either a lab­o­ra­to­ry test or a clin­i­cian diag­no­sis, is per­ma­nent­ly dis­qual­i­fy­ing ...” the memo reads.

    “Dur­ing the screen­ing process, a report­ed his­to­ry of con­firmed COVID-19 will be anno­tat­ed ‘Con­sid­ered dis­qual­i­fy­ing’“ pic.twitter.com/ZKx91AUbXo— Free (@Nathaniel_Free) May 4, 2020

    The memo is authen­tic, Pen­ta­gon spokes­woman Jes­si­ca Maxwell con­firmed to Mil­i­tary Times.

    Specif­i­cal­ly, it lays out guide­lines for MEPS staff to deal with poten­tial, as well as con­firmed, coro­n­avirus cas­es. That starts with screen­ing at all MEPS, which includes tak­ing a tem­per­a­ture and answer­ing ques­tions about symp­toms and poten­tial con­tact.

    If an appli­cant fails screen­ing, accord­ing to the memo, they won’t be test­ed, but they can return in 14 days if they’re symp­tom-free. Any­one who has been diag­nosed with COVID-19 will have to wait until 28 days after diag­no­sis to report to MEPS.

    Upon return, a diag­no­sis will be marked as “per­ma­nent­ly dis­qual­i­fy­ing” for acces­sion. Recruits can apply for waivers for all per­ma­nent­ly dis­qual­i­fy­ing con­di­tions, includ­ing sur­viv­ing COVID-19. How­ev­er, with­out any fur­ther guid­ance for excep­tions deal­ing with COVID-19, a review author­i­ty would have no jus­ti­fi­ca­tion to grant a waiv­er.

    Maxwell declined to explain why a coro­n­avirus diag­no­sis would be per­ma­nent­ly dis­qual­i­fy­ing, com­pared to oth­er viral, non-chron­ic ill­ness­es that do not pre­clude mil­i­tary ser­vice.

    How­ev­er, giv­en the lim­it­ed research on COVID-19, there are like­ly a few fac­tors that mil­i­tary med­ical pro­fes­sion­als are try­ing to hash out when it comes to recruit­ing sur­vivors: Whether res­pi­ra­to­ry dam­age from the virus is long-last­ing or per­ma­nent, and whether that can be assessed; the like­li­hood of recur­ring flare-ups, even if some­one has had two con­sec­u­tive neg­a­tive tests; and the pos­si­bil­i­ty that one bout of COVID-19 might not pro­vide full immu­ni­ty for the future, and could poten­tial­ly leave some­one at a high­er risk to con­tract it again, per­haps with worse com­pli­ca­tions.

    ...

    In recent weeks, new trainees have been 100-per­cent test­ed for COVID-19 before start­ing train­ing. So far, clus­ters have been dis­cov­ered at Fort Jack­son, South Car­oli­na, and Marine Corps Recruit Depot San Diego, the Army and Marine Corps’ biggest ini­tial entry train­ing instal­la­tions.

    ———-

    “Coro­n­avirus sur­vivors banned from join­ing the mil­i­tary” by Meghann Myers; Mil­i­tary Times; 05/06/2020

    ““Dur­ing the med­ical his­to­ry inter­view or exam­i­na­tion, a his­to­ry of COVID-19, con­firmed by either a lab­o­ra­to­ry test or a clin­i­cian diag­no­sis, is per­ma­nent­ly dis­qual­i­fy­ing ...” the memo reads.”

    A per­ma­nent dis­qual­i­fi­ca­tion for join­ing the mil­i­tary. That’s the cur­rent guide­line for any­one with a his­to­ry of COVID-19. Why such an extreme response to a dis­ease that appears to be large­ly a mild infec­tion for the vast major­i­ty of young adults? Espe­cial­ly if infec­tion can con­fer immu­ni­ty? Well, there still remain a num­ber of open ques­tions about the long-term health con­se­quences of an infec­tion. Open ques­tions like whether or not peo­ple can even get immu­ni­ty. Or if there’s per­ma­nent lung dam­age:

    ...
    Maxwell declined to explain why a coro­n­avirus diag­no­sis would be per­ma­nent­ly dis­qual­i­fy­ing, com­pared to oth­er viral, non-chron­ic ill­ness­es that do not pre­clude mil­i­tary ser­vice.

    How­ev­er, giv­en the lim­it­ed research on COVID-19, there are like­ly a few fac­tors that mil­i­tary med­ical pro­fes­sion­als are try­ing to hash out when it comes to recruit­ing sur­vivors: Whether res­pi­ra­to­ry dam­age from the virus is long-last­ing or per­ma­nent, and whether that can be assessed; the like­li­hood of recur­ring flare-ups, even if some­one has had two con­sec­u­tive neg­a­tive tests; and the pos­si­bil­i­ty that one bout of COVID-19 might not pro­vide full immu­ni­ty for the future, and could poten­tial­ly leave some­one at a high­er risk to con­tract it again, per­haps with worse com­pli­ca­tions.
    ...

    Now, it’s impor­tant to point out that COVID-19 is the name for the dis­ease caused by the SARS-CoV­‑2 virus so it’s pos­si­ble for some­one to be infect­ed by the virus and not man­i­fest COVID-19. In oth­er words, if a can­di­date recruit has has the SARS-CoV­‑2 anti­bod­ies, but not an actu­al COVID-19 case his­to­ry, they will still be eli­gi­ble for recruit­ment. That’s what the Pen­ta­gon appeared to con­firm to Talk­ing Points Memo in the fol­low­ing piece: some­one needs to have been hos­pi­tal­ized with COVID-19 for the ban to apply. The Pen­ta­gon also con­firmed that this is just an “inter­im” pol­i­cy and a per­ma­nent pol­i­cy is under devel­op­ment. So, again, we real­ly have to hope this move is being made out of an abun­dance of cau­tion due to a lack of infor­ma­tion on the long-term effects of the dis­ease and not due to them mil­i­tary gath­er­ing evi­dence that the dis­ease real­ly is per­ma­nent­ly dam­ag­ing oth­er­wise young and healthy peo­ple in large enough num­bers to jus­ti­fy make kind of blan­ket ban:

    Talk­ing Points Memo

    Mil­i­tary Bans COVID Sur­vivors From Enlist­ing

    By Josh Koven­sky
    May 7, 2020 11:56 a.m.

    The Pen­ta­gon has banned sur­vivors of COVID-19 from enlist­ing in the mil­i­tary, accord­ing to a gov­ern­ment memo released this week.

    A Pen­ta­gon spokes­woman con­firmed the doc­u­ment is authen­tic, describ­ing the ban to TPM as “inter­im.”

    A per­ma­nent pol­i­cy is cur­rent­ly being devel­oped, the spokes­woman told TPM.

    ...

    A Pen­ta­gon spokes­woman told TPM that, per the reg­u­la­tions, “any­body that has been hos­pi­tal­ized with COVID-19 will be med­ical­ly dis­qual­i­fied and would need a ser­vice waiv­er to join the mil­i­tary.

    Oth­er pri­or con­di­tions that the Pen­ta­gon con­sid­ers dis­qual­i­fy­ing with­out a waiv­er include recur­rent pneu­mo­nia, inflam­ma­tion of the heart, and kid­ney injuries requir­ing dial­y­sis.

    The memo itself states that the mil­i­tary will treat COVID-19 as a “3P” con­di­tion. Under the military’s med­ical pro­fil­ing sys­tem, that indi­cates a dis­qual­i­fy­ing defect in the applicant’s phys­i­cal capac­i­ty or sta­mi­na.

    “Dur­ing the med­ical his­to­ry inter­view or exam­i­na­tion, a his­to­ry of COVID-19, con­firmed by either a lab­o­ra­to­ry test or clin­i­cian diag­no­sis, is per­ma­nent­ly dis­qual­i­fy­ing,” the mem­o­ran­dum reads.

    The Pen­ta­gon declined to say why it believes COVID-19 to be per­ma­nent­ly dis­qual­i­fy­ing, or when it would issue per­ma­nent guid­ance on the issue.

    As doc­tors con­tin­ue to learn more about the ill­ness, seri­ous ques­tions linger over the longer-term effects of a COVID infec­tion. Some sur­vivors have report­ed reduced lung capac­i­ty, while oth­ers who found them­selves in grave con­di­tion emerge from the infec­tion with kid­ney fail­ure.

    ———–

    “Mil­i­tary Bans COVID Sur­vivors From Enlist­ing” by Josh Koven­sky; Talk­ing Points Memo; 05/07/2020

    “A Pen­ta­gon spokes­woman told TPM that, per the reg­u­la­tions, “any­body that has been hos­pi­tal­ized with COVID-19 will be med­ical­ly dis­qual­i­fied and would need a ser­vice waiv­er to join the mil­i­tary.””

    Hos­pi­tal­iza­tion appears to be required for the ban to apply. Which makes sense if you’re going to do a COVID ban because almost all young adults is going to get exposed to the virus even­tu­al­ly and most of them have very mild symp­toms that don’t require hos­pi­tal­iza­tion. Hope­ful­ly this rule isn’t inad­ver­tent­ly going to end up encour­ag­ing aspir­ing recruits to not go to the hos­pi­tal if they get sick with COVID-like symp­toms this sum­mer. And, again, hope­ful­ly this rules isn’t based on inter­nal med­ical data the mil­i­tary has col­lect­ed on the long-term con­se­quences of COVID-19 on the rel­a­tive­ly young and healthy.

    Final­ly, here’s a Vox arti­cle that com­piles what it known so far about the pos­si­ble long-term con­se­quences of COVID-19 cas­es. Unfor­tu­nate­ly, based on the data we have so far, it sounds like the Pen­tagon’s deci­sion to impose a life-time ban on peo­ple hos­pi­tal­ized for COVID-19 might make sense for an insti­tu­tion like the mil­i­tary because there are a lot of reports of rel­a­tive­ly young peo­ple who get sick and are poten­tial­ly deal­ing with life-long con­se­quences. A shock­ing­ly broad array of life-long con­se­quences:

    Vox

    The emerg­ing long-term com­pli­ca­tions of Covid-19, explained

    “It is a true roller coast­er of symp­toms and sever­i­ties, with each new day offer­ing many unknowns.”

    By Lois Parsh­ley
    May 8, 2020, 1:10pm EDT

    At first, Lau­ren Nichols tried to explain away her symp­toms. In ear­ly March, the healthy 32-year-old felt an intense burn­ing sen­sa­tion, like acid reflux, when she breathed. Embar­rassed, she didn’t ini­tial­ly seek med­ical care. When her short­ness of breath kept get­ting worse, her doc­tor test­ed her for Covid-19.

    Her results came back pos­i­tive. But for Nichols, that was just the begin­ning. Over the next eight weeks, she devel­oped wide and var­ied symp­toms, includ­ing extreme and chron­ic fatigue, diar­rhea, nau­sea, tremors, headaches, dif­fi­cul­ty con­cen­trat­ing, and short-term mem­o­ry loss.

    “The guide­lines that were pro­vid­ed by the CDC [Cen­ters for Dis­ease Con­trol and Pre­ven­tion] were not appro­pri­ate­ly cap­tur­ing the symp­toms that I was expe­ri­enc­ing, which in turn meant that the med­ical com­mu­ni­ty was unable to ‘val­i­date’ my symp­toms,” she says. “This became a vicious cycle of doubt, con­fu­sion, and lone­li­ness.”

    Some­where between 5 and 80 per­cent of peo­ple who test pos­i­tive for Covid-19 may be asymp­to­matic, or only devel­op symp­toms days or even weeks after their test, and many of these peo­ple will have a mild form of the ill­ness with no last­ing symp­toms. But Nichols is one of many Covid-19 patients who are find­ing their recov­ery takes far longer than the two weeks the World Health Orga­ni­za­tion says peo­ple with mild cas­es can expect. (The WHO says those with severe or crit­i­cal cas­es can expect three to six weeks of recov­ery.)

    Because Covid-19 is a new dis­ease, there are no stud­ies about its long-term tra­jec­to­ry for those with more severe symp­toms; even the ear­li­est patients to recov­er in Chi­na were only infect­ed a few months ago. But doc­tors say the nov­el coro­n­avirus can attach to human cells in many parts of the body and pen­e­trate many major organs, includ­ing the heart, kid­neys, brain, and even blood ves­sels.

    “The dif­fi­cul­ty is sort­ing out long-term con­se­quences,” says Joseph Bren­nan, a car­di­ol­o­gist at the Yale School of Med­i­cine. While some patients may ful­ly recov­er, he and oth­er experts wor­ry oth­ers will suf­fer long-term dam­age, includ­ing lung scar­ring, heart dam­age, and neu­ro­log­i­cal and men­tal health effects.

    The UK Nation­al Health Ser­vice assumes that of Covid-19 patients who have required hos­pi­tal­iza­tion, 45 per­cent will need ongo­ing med­ical care, 4 per­cent will require in-patient reha­bil­i­ta­tion, and 1 per­cent will per­ma­nent­ly require acute care. Oth­er pre­lim­i­nary evi­dence, as well as his­tor­i­cal research on oth­er coro­n­avirus­es like severe acute res­pi­ra­to­ry syn­drome (SARS) and Mid­dle East res­pi­ra­to­ry syn­drome (MERS), sug­gests that for some peo­ple, a full recov­ery might still be years off. For oth­ers, there may be no return­ing to nor­mal.

    There’s a lot we still don’t know, but here are a few of the most notable poten­tial long-term impacts that are already show­ing up in some Covid-19 patients.

    Lung scar­ring

    Melanie Mon­tano, 32, who test­ed pos­i­tive for Covid-19 in March, says that more than sev­en weeks after she first got sick, she still expe­ri­ences symp­toms on and off, includ­ing burn­ing in her lungs and a dry cough.

    Bren­nan says symp­toms like that occur because “this virus cre­ates an incred­i­bly aggres­sive immune response, so spaces [in the lungs] are filled with debris and pus, mak­ing your lungs less pli­able.”

    On CT scans, while nor­mal lungs appear black, Covid-19 patients’ lungs fre­quent­ly have lighter gray patch­es, called “ground-glass opac­i­ties” — which may not heal.

    One study from Chi­na found that this ground-glass appear­ance showed up in scans of 77 per­cent of Covid-19 patients. In anoth­er study out of Chi­na, pub­lished in Radi­ol­o­gy, 66 of 70 hos­pi­tal­ized patients had some amount of lung dam­age in CT scans, and more than half had the kind of lesions that are like­ly to devel­op into scars. (A third study from Chi­na sug­gests this is not just for crit­i­cal­ly ill patients; its authors found that of 58 asymp­to­matic patients, 95 per­cent also had evi­dence of these ground-glass opac­i­ties in their lungs. More than a quar­ter of these indi­vid­u­als went on to devel­op symp­toms with­in a few days.)

    “These kinds of tis­sue changes can cause per­ma­nent dam­age,” says Ali Gho­lam­rezanezhad, a radi­ol­o­gist at the Keck School of Med­i­cine at the Uni­ver­si­ty of South­ern Cal­i­for­nia.

    Although it’s still too ear­ly to know if patients with ongo­ing lung symp­toms like Mon­tano will have per­ma­nent lung dam­age, doc­tors can learn more about what to expect from look­ing back to peo­ple who have recov­ered from SARS and MERS, oth­er coro­n­avirus­es that result­ed in sim­i­lar lung tis­sue changes.

    One small lon­gi­tu­di­nal study pub­lished in Nature fol­lowed 71 SARS patients from 2003 until 2018 and found that more than a third had resid­ual scar­ring, which can mean reduced lung capac­i­ty. MERS is a lit­tle hard­er to extrap­o­late from, since few­er than 2,500 peo­ple were infect­ed, and some­where between 30 and 40 per­cent died. But one study found that about a third of 36 MERS sur­vivors also had long-term lung dam­age.

    Gho­lam­rezanezhad has recent­ly done a lit­er­a­ture review of SARS and MERS and says that for this sub­set of peo­ple, “The pul­monary func­tion nev­er comes back; their abil­i­ty to do nor­mal activ­i­ties nev­er goes back to base­line.”

    Addi­tion­al­ly, Covid-19 scar­ring rates may end up being high­er than SARS and MERS patients because those ill­ness­es often attacked only one lung. But Covid-19 appears to often affect both lungs, which Gho­lam­rezanezhad says esca­lates the risks of lung scar­ring.

    He has already seen resid­ual scar­ring in Covid-19 patients and is now design­ing a study to iden­ti­fy what fac­tors might make some peo­ple at high­er risk of per­ma­nent dam­age. He sus­pects hav­ing any type of under­ly­ing lung dis­ease, like asth­ma, or oth­er health con­di­tions, like hyper­ten­sion, might increase the risk of hav­ing longer-term lung issues. Addi­tion­al­ly, “the old­er you are, prob­a­bly the high­er your chance of scar­ring,” he says.

    For peo­ple with this kind of lung scar­ring, nor­mal activ­i­ties may become more chal­leng­ing. “Rou­tine things, like run­ning up a flight of stairs, would leave these indi­vid­u­als gasp­ing for air,” Bren­nan says.

    Stroke, embolisms, and blood clot­ting

    Many patients hos­pi­tal­ized for Covid-19 are expe­ri­enc­ing unex­pect­ed­ly high rates of blood clots, like­ly due to inflam­ma­to­ry respons­es to the infec­tion. These can cause lung block­ages, strokes, heart attacks, and oth­er com­pli­ca­tions with seri­ous, last­ing effects.

    Blood clots that form in or reach the brain can cause a stroke. Although strokes are more typ­i­cal­ly seen in old­er peo­ple, strokes are now being report­ed even in young Covid-19 patients. In Wuhan, Chi­na, about 5 per­cent of hos­pi­tal­ized Covid-19 patients had strokes, and a sim­i­lar pat­tern was report­ed with SARS.

    In younger peo­ple who have strokes, mor­tal­i­ty rates are rel­a­tive­ly low com­pared to those who are old­er, and many peo­ple recov­er. But stud­ies show only between 42 and 53 per­cent are able to return to work.

    Blood clots can also cut off cir­cu­la­tion to part of the lungs, a con­di­tion known as a pul­monary embolism, which can be dead­ly. In France, two stud­ies sug­gest that between 23 and 30 per­cent of peo­ple with severe Covid-19 are also hav­ing pul­monary embolisms.

    One analy­sis found that after a pul­monary embolism, “symp­toms and func­tion­al lim­i­ta­tions are fre­quent­ly report­ed by sur­vivors.” These include fatigue, heart pal­pi­ta­tions, short­ness of breath, marked lim­i­ta­tion of phys­i­cal activ­i­ty, and inabil­i­ty to do phys­i­cal activ­i­ty with­out dis­com­fort.

    Blood clots in oth­er major organs can also cause seri­ous prob­lems. Renal fail­ure has been a com­mon chal­lenge in many severe Covid-19 patients, and patients’ clot­ted blood has been clog­ging dial­y­sis machines. Some of these acute kid­ney injuries may be per­ma­nent, requir­ing ongo­ing dial­y­sis.

    Clots not in organs can be seri­ous, too. Deep vein throm­bo­sis, for exam­ple, occurs when a blood clot forms in a vein, often the legs. Nick Cordero, a Tony-nom­i­nat­ed Broad­way and tele­vi­sion actor, recent­ly had to have his right leg ampu­tat­ed after Covid-relat­ed blood clots.

    Abnor­mal blood clot­ting even seems to be hap­pen­ing in peo­ple after they’ve appeared to recov­er. One 32-year-old woman in Chica­go, for exam­ple, had been dis­charged from the hos­pi­tal for a week when she died sud­den­ly with a severe­ly swollen leg, a sign of deep vein throm­bo­sis, accord­ing to local broad­cast­er WGN9. Or take Troy Ran­dle, a 49-year-old car­di­ol­o­gist in New Jer­sey, who was declared safe to go back to work after recov­er­ing from Covid-19 when he devel­oped a vicious headache. A CT scan con­firmed he’d had a stroke.

    Although there’s still a short­age of data, one study found that as many as 31 per­cent of ICU patients with Covid-19 infec­tions had these kinds of clot­ting prob­lems. In the mean­time, the Inter­na­tion­al Soci­ety on Throm­bo­sis and Haemosta­sis has issued guide­lines that recov­ered Covid-19 patients should con­tin­ue tak­ing anti­co­ag­u­lants even after being dis­charged from the hos­pi­tal.

    Heart dam­age

    Being crit­i­cal­ly ill, espe­cial­ly with low oxy­gen lev­els, puts addi­tion­al stress on the heart. But doc­tors now think that in Covid-19 patients, viral par­ti­cles might also be specif­i­cal­ly inflam­ing the heart mus­cle. (The heart has many ACE2 recep­tors.)

    “In Chi­na, doc­tors not­ed some peo­ple com­ing [in] with chest pain,” says Mitchell Elkind, pres­i­dent-elect of the Amer­i­can Heart Asso­ci­a­tion and pro­fes­sor of neu­rol­o­gy and epi­demi­ol­o­gy at Colum­bia Uni­ver­si­ty. “They had a heart attack, and then devel­oped Covid symp­toms or test­ed pos­i­tive after.”

    One study from Wuhan in Jan­u­ary found that 12 per­cent of Covid-19 patients had signs of car­dio­vas­cu­lar dam­age. These patients had high­er lev­els of tro­ponin, a pro­tein released in the blood by an injured heart mus­cle. Since then, oth­er reports sug­gest the virus may direct­ly cause acute myocardi­tis and heart fail­ure. (Heart fail­ure was also seen with MERS and is known to be cor­re­lat­ed with even the sea­son­al flu.)

    In March, anoth­er study looked at 416 hos­pi­tal­ized Covid-19 patients and found that 19 per­cent showed signs of heart dam­age. Uni­ver­si­ty of Texas Health Sci­ence Cen­ter researchers warn that in sur­vivors, Covid-19 may cause lin­ger­ing car­diac dam­age, as well as mak­ing exist­ing car­dio­vas­cu­lar prob­lems worse, fur­ther increas­ing the risk for heart attack and stroke.

    A pul­monary crit­i­cal care doc­tor at Mount Sinai Hos­pi­tal in New York City, for exam­ple, recov­ered from Covid-19, only to learn she had devel­oped car­diomy­opa­thy, a con­di­tion where your heart has trou­ble deliv­er­ing blood around your body. Although pre­vi­ous­ly healthy, when she returned to work, she told NBC, “I couldn’t run around like I always do.”

    The spe­cif­ic con­se­quences may vary depend­ing on how the heart is affect­ed. For exam­ple, Covid-19 has been linked to myocardi­tis, a con­di­tion where inflam­ma­tion weak­ens the heart, cre­ates scar tis­sue, and makes it work hard­er to cir­cu­late the body’s oxy­gen. The Myocardi­tis Foun­da­tion rec­om­mends these patients avoid cig­a­rettes and alco­hol, and stay away from rig­or­ous exer­cise until approved by their doc­tor.

    Neu­rocog­ni­tive and men­tal health impacts

    Covid-19 also seems to affect the cen­tral ner­vous sys­tem, with poten­tial­ly long-last­ing con­se­quences. In one study from Chi­na, more than a third of 214 peo­ple hos­pi­tal­ized with con­firmed Covid-19 had neu­ro­log­i­cal symp­toms, includ­ing dizzi­ness, headaches, impaired con­scious­ness, vision, taste/smell impair­ment, and nerve pain while they were ill. These symp­toms were more com­mon in patients with severe cas­es, where the inci­dence increased to 46.5 per­cent. Anoth­er study in France found neu­ro­log­ic fea­tures in 58 of 64 crit­i­cal­ly ill Covid-19 patients.

    As the pan­dem­ic goes on, Elkind says, “We need to be on the look­out for long-term neu­rocog­ni­tive prob­lems.”

    Look­ing back to SARS and MERS sug­gests that Covid-19 patients may have slight­ly delayed onset of neu­ro­log­i­cal impacts. Andrew Joseph­son, a doc­tor at the Uni­ver­si­ty of Cal­i­for­nia San Fran­cis­co, wrote in JAMA, “Although the SARS epi­dem­ic was lim­it­ed to about 8,000 patients world­wide, there were some lim­it­ed reports of neu­ro­log­ic com­pli­ca­tions of SARS that appeared in patients 2 to 3 weeks into the course of the ill­ness.” These includ­ed mus­cu­lar weak­ness, burn­ing or prick­ling, and numb­ness, and the break­down of mus­cle tis­sue into the blood. Neu­ro­log­i­cal injuries, includ­ing impaired bal­ance and coor­di­na­tion, con­fu­sion, and coma, were also found with MERS.

    Long-term com­pli­ca­tions of Covid-19 — whether caused by the virus itself or the inflam­ma­tion it trig­gers — could include decreased atten­tion, con­cen­tra­tion, and mem­o­ry, as well as dys­func­tion in periph­er­al nerves, “the ones that go to your arms, legs, fin­gers, and toes,” Elkind says.

    There are oth­er cog­ni­tive impli­ca­tions for peo­ple who receive inten­sive treat­ment in hos­pi­tals. For exam­ple, delir­i­um — an acute­ly dis­turbed state of mind that can result in con­fu­sion and see­ing or hear­ing things that aren’t there — affects about two-thirds of patients in ICUs, and research sug­gests the pres­ence of delir­i­um dur­ing severe ill­ness pre­dicts future long-term cog­ni­tive decline.

    Pre­vi­ous research on acute res­pi­ra­to­ry dis­tress syn­drome (ARDS) more gen­er­al­ly may also pro­vide clues to what neu­ro­log­i­cal issues crit­i­cal­ly ill Covid-19 patients might see after leav­ing the hos­pi­tal.

    Research shows one in five ARDS sur­vivors expe­ri­ences long-term cog­ni­tive impair­ment even five years after being dis­charged. Con­tin­u­ing impair­ments can include short-term mem­o­ry prob­lems and dif­fi­cul­ty with learn­ing and exec­u­tive func­tion. These can lead to chal­lenges like dif­fi­cul­ty work­ing, impaired mon­ey man­age­ment, or strug­gling to per­form dai­ly tasks.

    ARDS sur­vivors fre­quent­ly have increased rates of depres­sion and anx­i­ety, and many expe­ri­ence post-trau­mat­ic stress. Although it’s still too ear­ly to have much data on Covid-19, dur­ing the SARS out­break, for­mer patients strug­gled with psy­cho­log­i­cal dis­tress and stress for at least a year after the out­break.

    “I felt impris­oned with­in my body, impris­oned with­in my home, and tremen­dous­ly ignored and mis­un­der­stood by the gen­er­al pub­lic, and even those clos­est to me,” Nichols says about her bat­tle with Covid-19. “I feel incred­i­bly alone.”

    Jane, who prefers to use a pseu­do­nym because she fears ret­ri­bu­tion at the hos­pi­tal where she works, test­ed pos­i­tive for Covid-19 more than a month ago. She’s still strug­gling with fevers, heart issues, and neu­ro­log­i­cal issues, but the most dif­fi­cult part, she says, is how tired she is of “being treat­ed like I am a bomb that no one knows how to dis­arm.” Jane, a nurse who cared for AIDS patients dur­ing the ’90s, says, “This is exact­ly what those peo­ple went through. There is a ter­ri­ble stig­ma.” In addi­tion to the stig­ma, uncer­tain­ty has added to her men­tal health bur­den.

    “Peo­ple need to know this dis­ease can linger and wreck your life and health,” she says. “And no one knows what to do for us.”

    Child­hood inflam­ma­tion, male infer­til­i­ty, and oth­er pos­si­ble last­ing effects

    The nov­el coro­n­avirus con­tin­ues to frus­trate sci­en­tists and patients alike with its mys­ter­ies. One of these is a small but grow­ing num­ber of chil­dren who recent­ly began show­ing up at doc­tors’ offices in Britain, Italy, and Spain with strange symp­toms, includ­ing a rash, a high fever, and heart inflam­ma­tion.

    On May 4, the New York City Health Depart­ment not­ed that at least 15 chil­dren with these symp­toms had been hos­pi­tal­ized there, too. These cas­es present like a severe immune response called Kawasa­ki dis­ease, where blood ves­sels can begin to leak, and flu­id builds up in the lungs and oth­er major organs. Although only some of these chil­dren have test­ed pos­i­tive for Covid-19, Rus­sell Vin­er, pres­i­dent of the Roy­al Col­lege of Pedi­atrics and Child Health, told the New York Times, “the work­ing hypoth­e­sis is that it’s Covid-relat­ed.”

    Chil­dren who sur­vive Kawasa­ki-like con­di­tions can suf­fer myocar­dial and vas­cu­lar com­pli­ca­tions in adult­hood. But it’s too ear­ly to know how Covid-relat­ed cas­es will devel­op. Many of the small num­ber of report­ed cas­es appear to be respond­ing well to treat­ment.

    Oth­er researchers are sug­gest­ing that Covid-19 may pose par­tic­u­lar prob­lems for men beyond their dis­pro­por­tion­ate mor­tal­i­ty from the ill­ness. The tes­ti­cles con­tain a high num­ber of ACE2 recep­tors, explained Ali Raba, in a recent let­ter to the World Jour­nal of Urol­o­gy. “There is a the­o­ret­i­cal pos­si­bil­i­ty that Covid-19 has the poten­tial to cause male infer­til­i­ty.” Anoth­er study, look­ing at 38 patients in Chi­na who had been severe­ly ill with Covid-19, found that dur­ing their ill­ness, 15 had virus RNA in their semen sam­ples, as well as two of 23 recov­er­ing patients. (The pres­ence of viral RNA doesn’t nec­es­sar­i­ly indi­cate infec­tious capac­i­ty.)

    Anoth­er recent study also showed that in 81 men with Covid-19, male hor­mone ratios were off, which could sig­nal trou­ble for fer­til­i­ty down the line. The authors called for more atten­tion to be paid, par­tic­u­lar­ly on “repro­duc­tive-aged men.” An April 20 paper pub­lished in Nature went so far as to sug­gest, “After recov­ery from COVID-19, young men who are inter­est­ed in hav­ing chil­dren should receive a con­sul­ta­tion regard­ing their fer­til­i­ty.”

    And we are just at the begin­ning of fig­ur­ing out what this com­plex infec­tion means for oth­er organ sys­tems and their recov­ery. For exam­ple, a recent preprint from Chi­nese doc­tors looked at 34 Covid-19 sur­vivors’ blood. While they saw a dif­fer­ence between severe and mild cas­es, the researchers found that regard­less of the sever­i­ty of the dis­ease, after recov­ered patients were dis­charged from the hos­pi­tal, many bio­log­i­cal mea­sures “failed to return to nor­mal.” The most con­cern­ing mea­sures sug­gest­ed ongo­ing impaired liv­er func­tion.

    ...

    ———–

    “The emerg­ing long-term com­pli­ca­tions of Covid-19, explained” by Lois Parsh­ley; Vox; 05/08/2020

    “Because Covid-19 is a new dis­ease, there are no stud­ies about its long-term tra­jec­to­ry for those with more severe symp­toms; even the ear­li­est patients to recov­er in Chi­na were only infect­ed a few months ago. But doc­tors say the nov­el coro­n­avirus can attach to human cells in many parts of the body and pen­e­trate many major organs, includ­ing the heart, kid­neys, brain, and even blood ves­sels.

    As the evi­dence keeps com­ing in with one unex­pect­ed symp­tom after anoth­er one find­ing is becom­ing increas­ing­ly clear: This virus attacks the whole body. It’s a find­ing unfor­tu­nate­ly reflect­ed in the remark­able diver­si­ty of symp­toms expe­ri­enced by patients even after leav­ing the hos­pi­tal. And that includes “ground-class” signs of scar­ring in the lungs of asymp­to­matic patients:

    ...
    The UK Nation­al Health Ser­vice assumes that of Covid-19 patients who have required hos­pi­tal­iza­tion, 45 per­cent will need ongo­ing med­ical care, 4 per­cent will require in-patient reha­bil­i­ta­tion, and 1 per­cent will per­ma­nent­ly require acute care. Oth­er pre­lim­i­nary evi­dence, as well as his­tor­i­cal research on oth­er coro­n­avirus­es like severe acute res­pi­ra­to­ry syn­drome (SARS) and Mid­dle East res­pi­ra­to­ry syn­drome (MERS), sug­gests that for some peo­ple, a full recov­ery might still be years off. For oth­ers, there may be no return­ing to nor­mal.

    ...

    On CT scans, while nor­mal lungs appear black, Covid-19 patients’ lungs fre­quent­ly have lighter gray patch­es, called “ground-glass opac­i­ties” — which may not heal.

    One study from Chi­na found that this ground-glass appear­ance showed up in scans of 77 per­cent of Covid-19 patients. In anoth­er study out of Chi­na, pub­lished in Radi­ol­o­gy, 66 of 70 hos­pi­tal­ized patients had some amount of lung dam­age in CT scans, and more than half had the kind of lesions that are like­ly to devel­op into scars. (A third study from Chi­na sug­gests this is not just for crit­i­cal­ly ill patients; its authors found that of 58 asymp­to­matic patients, 95 per­cent also had evi­dence of these ground-glass opac­i­ties in their lungs. More than a quar­ter of these indi­vid­u­als went on to devel­op symp­toms with­in a few days.)

    “These kinds of tis­sue changes can cause per­ma­nent dam­age,” says Ali Gho­lam­rezanezhad, a radi­ol­o­gist at the Keck School of Med­i­cine at the Uni­ver­si­ty of South­ern Cal­i­for­nia.
    ...

    There’s the range of car­diopul­monary com­pli­ca­tions like blood clot­ting that, in turn, can inflict per­ma­nent dam­age on the body:

    ...

    Blood clots that form in or reach the brain can cause a stroke. Although strokes are more typ­i­cal­ly seen in old­er peo­ple, strokes are now being report­ed even in young Covid-19 patients. In Wuhan, Chi­na, about 5 per­cent of hos­pi­tal­ized Covid-19 patients had strokes, and a sim­i­lar pat­tern was report­ed with SARS.

    ...

    Blood clots can also cut off cir­cu­la­tion to part of the lungs, a con­di­tion known as a pul­monary embolism, which can be dead­ly. In France, two stud­ies sug­gest that between 23 and 30 per­cent of peo­ple with severe Covid-19 are also hav­ing pul­monary embolisms.

    ...

    Blood clots in oth­er major organs can also cause seri­ous prob­lems. Renal fail­ure has been a com­mon chal­lenge in many severe Covid-19 patients, and patients’ clot­ted blood has been clog­ging dial­y­sis machines. Some of these acute kid­ney injuries may be per­ma­nent, requir­ing ongo­ing dial­y­sis.

    ...

    Abnor­mal blood clot­ting even seems to be hap­pen­ing in peo­ple after they’ve appeared to recov­er. One 32-year-old woman in Chica­go, for exam­ple, had been dis­charged from the hos­pi­tal for a week when she died sud­den­ly with a severe­ly swollen leg, a sign of deep vein throm­bo­sis, accord­ing to local broad­cast­er WGN9. Or take Troy Ran­dle, a 49-year-old car­di­ol­o­gist in New Jer­sey, who was declared safe to go back to work after recov­er­ing from Covid-19 when he devel­oped a vicious headache. A CT scan con­firmed he’d had a stroke.

    ...

    Being crit­i­cal­ly ill, espe­cial­ly with low oxy­gen lev­els, puts addi­tion­al stress on the heart. But doc­tors now think that in Covid-19 patients, viral par­ti­cles might also be specif­i­cal­ly inflam­ing the heart mus­cle. (The heart has many ACE2 recep­tors.)

    ...

    One study from Wuhan in Jan­u­ary found that 12 per­cent of Covid-19 patients had signs of car­dio­vas­cu­lar dam­age. These patients had high­er lev­els of tro­ponin, a pro­tein released in the blood by an injured heart mus­cle. Since then, oth­er reports sug­gest the virus may direct­ly cause acute myocardi­tis and heart fail­ure. (Heart fail­ure was also seen with MERS and is known to be cor­re­lat­ed with even the sea­son­al flu.)

    In March, anoth­er study looked at 416 hos­pi­tal­ized Covid-19 patients and found that 19 per­cent showed signs of heart dam­age. Uni­ver­si­ty of Texas Health Sci­ence Cen­ter researchers warn that in sur­vivors, Covid-19 may cause lin­ger­ing car­diac dam­age, as well as mak­ing exist­ing car­dio­vas­cu­lar prob­lems worse, fur­ther increas­ing the risk for heart attack and stroke.
    ...

    Then there’s the pos­si­ble neu­rocog­ni­tive dam­age. We don’t know yet what that dam­age might be, but symp­toms like decreased atten­tion, con­cen­tra­tion, mem­o­ry, or nerve dam­age are a real pos­si­bil­i­ty. And for the severe­ly ill who have to endure the kind of trau­mat­ic expe­ri­ence like being hooked up to ven­ti­la­tor for days for weeks on end, there’s the real pos­si­bil­i­ty of addi­tion­al long-term cog­ni­tive impair­ment and PTSD:

    ...

    Long-term com­pli­ca­tions of Covid-19 — whether caused by the virus itself or the inflam­ma­tion it trig­gers — could include decreased atten­tion, con­cen­tra­tion, and mem­o­ry, as well as dys­func­tion in periph­er­al nerves, “the ones that go to your arms, legs, fin­gers, and toes,” Elkind says.

    There are oth­er cog­ni­tive impli­ca­tions for peo­ple who receive inten­sive treat­ment in hos­pi­tals. For exam­ple, delir­i­um — an acute­ly dis­turbed state of mind that can result in con­fu­sion and see­ing or hear­ing things that aren’t there — affects about two-thirds of patients in ICUs, and research sug­gests the pres­ence of delir­i­um dur­ing severe ill­ness pre­dicts future long-term cog­ni­tive decline.

    Pre­vi­ous research on acute res­pi­ra­to­ry dis­tress syn­drome (ARDS) more gen­er­al­ly may also pro­vide clues to what neu­ro­log­i­cal issues crit­i­cal­ly ill Covid-19 patients might see after leav­ing the hos­pi­tal.

    Research shows one in five ARDS sur­vivors expe­ri­ences long-term cog­ni­tive impair­ment even five years after being dis­charged. Con­tin­u­ing impair­ments can include short-term mem­o­ry prob­lems and dif­fi­cul­ty with learn­ing and exec­u­tive func­tion. These can lead to chal­lenges like dif­fi­cul­ty work­ing, impaired mon­ey man­age­ment, or strug­gling to per­form dai­ly tasks.

    ARDS sur­vivors fre­quent­ly have increased rates of depres­sion and anx­i­ety, and many expe­ri­ence post-trau­mat­ic stress. Although it’s still too ear­ly to have much data on Covid-19, dur­ing the SARS out­break, for­mer patients strug­gled with psy­cho­log­i­cal dis­tress and stress for at least a year after the out­break.
    ...

    Hor­mone lev­els can also be affect­ed, which could have a range of com­pli­ca­tions includ­ing fer­til­i­ty issues. But it’s also pos­si­ble the virus direct­ly attack tes­ti­cles, which hap­pen to have a high num­ber of ACE2 recep­tors. So there’s a range of ways this virus could impact fer­til­i­ty that we already know of which is a par­tic­u­lar­ly trou­bling find­ing giv­en the racial dis­par­i­ties of how this dis­ease is being felt. Caus­ing fer­til­i­ty issues in young males is the kind of ‘fea­ture’ that would make the spread of this virus even more tempt­ing for white nation­al­ists. And we already know in the US it’s dis­pro­por­tion­ate­ly poor minori­ties catch­ing the dis­ease since that group tends of have employ­ment where work­ing from home isn’t an option. How will a white nation­al­ist admin­is­tra­tion like the Trump admin­is­tra­tion respond if it learns this dis­ease is dis­pro­por­tion­ate­ly hit­ting minori­ties and caus­ing fer­til­i­ty issues? Because that’s the kind of viral ‘fea­ture’ some­one like, say, Steve Ban­non, would be dream­ing of spread­ing across the US if it could be done in a way that sys­tem­at­i­cal­ly tar­gets young minori­ties:

    ...
    Oth­er researchers are sug­gest­ing that Covid-19 may pose par­tic­u­lar prob­lems for men beyond their dis­pro­por­tion­ate mor­tal­i­ty from the ill­ness. The tes­ti­cles con­tain a high num­ber of ACE2 recep­tors, explained Ali Raba, in a recent let­ter to the World Jour­nal of Urol­o­gy. “There is a the­o­ret­i­cal pos­si­bil­i­ty that Covid-19 has the poten­tial to cause male infer­til­i­ty.” Anoth­er study, look­ing at 38 patients in Chi­na who had been severe­ly ill with Covid-19, found that dur­ing their ill­ness, 15 had virus RNA in their semen sam­ples, as well as two of 23 recov­er­ing patients. (The pres­ence of viral RNA doesn’t nec­es­sar­i­ly indi­cate infec­tious capac­i­ty.)

    Anoth­er recent study also showed that in 81 men with Covid-19, male hor­mone ratios were off, which could sig­nal trou­ble for fer­til­i­ty down the line. The authors called for more atten­tion to be paid, par­tic­u­lar­ly on “repro­duc­tive-aged men.” An April 20 paper pub­lished in Nature went so far as to sug­gest, “After recov­ery from COVID-19, young men who are inter­est­ed in hav­ing chil­dren should receive a con­sul­ta­tion regard­ing their fer­til­i­ty.”

    And we are just at the begin­ning of fig­ur­ing out what this com­plex infec­tion means for oth­er organ sys­tems and their recov­ery. For exam­ple, a recent preprint from Chi­nese doc­tors looked at 34 Covid-19 sur­vivors’ blood. While they saw a dif­fer­ence between severe and mild cas­es, the researchers found that regard­less of the sever­i­ty of the dis­ease, after recov­ered patients were dis­charged from the hos­pi­tal, many bio­log­i­cal mea­sures “failed to return to nor­mal.” The most con­cern­ing mea­sures sug­gest­ed ongo­ing impaired liv­er func­tion.
    ...

    So as that Vox arti­cle makes clear, the Pen­ta­gon does­n’t nec­es­sar­i­ly need to be sit­ting on inter­nal data on the med­ical con­se­quences for recov­ered COVID patients because the pub­licly avail­able data is already so omi­nous.

    In oth­er news, here’s an update on Pres­i­dent Trump’s inex­plic­a­ble deci­sion to give the com­mence­ment speech for this year’s grad­u­at­ing West Point class — a deci­sion that’s going to force 1,000 grad­u­at­ing seniors to trav­el back to New York to the cam­pus just 50 miles North of New York City: there is no update so we can only assume it’s still sched­uled for June. It’s the kind of sit­u­a­tion where the lack of new news should real­ly be news.

    Posted by Pterrafractyl | May 8, 2020, 2:01 pm
  7. Pres­i­dent Trump did it again: He said some­thing that makes is seem like he’s try­ing to ensure SARS-CoV­‑2 virus is allowed to spread unde­tect­ed as much as pos­si­ble as rapid­ly. Specif­i­cal­ly, Trump called coro­n­avirus test­ing “over­rat­ed” and sug­gest­ed that test­ing isn’t actu­al­ly use­ful because peo­ple can get infect­ed after they test neg­a­tive. And while it’s pos­si­ble Trump is new­ly enam­ored with the “herd immu­ni­ty” strat­e­gy of just let­ting the virus spread as rapid­ly as pos­si­ble in the hopes that every­one gains immu­ni­ty, keep in mind that if there were indeed ear­li­er undis­cov­ered (or undis­closed) out­breaks of this coro­n­avirus in the US in 2019 this strat­e­gy of encour­ag­ing the spread with­out test­ing could be an effec­tive way to obscure those ear­li­er out­breaks from being ret­ro­spec­tive­ly dis­cov­ered through phy­lo­ge­net­ic analy­sis of viral sequences. Espe­cial­ly if new­er strains of the virus have a demon­strat­ed capac­i­ty to become the dom­i­nant strain when they move into an area and effec­tive­ly replace old­er strains that may have been bub­bling under the sur­face.

    So with that in mind, here’s anoth­er study recent­ly came out about the emer­gence of dif­fer­ent strains of the SARS-CoV­‑2 virus. This one is from a lab Los Alam­os Nation­al Lab­o­ra­to­ry. Like many of the pre­vi­ous stud­ies track­ing the emer­gence and spread of dif­fer­ent strains this study was also based on phy­lo­ge­net­ic analy­sis of viral sequences found in the GISAID con­sor­tium. The team found that a par­tic­u­lar muta­tion on the ‘spike-pro­tien’ that arose in late Jan­u­ary rapid­ly came to dom­i­nate the pan­dem­ic in Europe and then the US East Coast pan­dem­ic and issued a warn­ing that could have big omi­nous impli­ca­tions for any “herd immu­ni­ty” strate­gies.

    Part of what makes this study inter­est­ing is they found that this new strain would rapid­ly replace the strains that were already in an area when it moved it accord­ing to their analy­sis. The authors say they repeat­ed­ly saw this hap­pen­ing in their analy­sis. Recall how, back in ear­ly March, a team out of Chi­na observed how mutant strain — they ‘L‑type’ strain — emerged in Wuhan in late Decem­ber and rapid­ly become the dom­i­nant strain in the Wuhan epi­dem­ic. Then there was the study out of Cam­bridge that iden­ti­fied three dis­tinct strains (Type A, B, and C), with Chi­na being pri­mar­i­ly hit by Type A at first. But then Type B strain emerged in Wuhan in Decem­ber and rapid­ly became the dom­i­nant strain there while spread­ing to Europe and even­tu­al­ly the US East Coast. The Type B strain appears to be the same as the ‘L‑type’ strain from the ear­li­er study based on the muta­tions the researchers used to define them.

    This lat­est study out of Los Alam­os appears to have arrived at a sim­i­lar con­clu­sion about a new strain emerg­ing that over­takes the pre­vi­ous strains in an area. Except in this case the new strain they iden­ti­fied emerged in late Jan­u­ary. The authors sug­gest that it either arose in Europe (specif­i­cal­ly Ger­many) or Wuhan in late Jan­u­ary and rapid­ly jumped to Europe. So it sounds like the last few months of the pan­dem­ic in the US and Europe have been heav­i­ly dom­i­nat­ed by a new strain that was first iden­ti­fied in late Jan­u­ary in Wuhan and Ger­many.

    Keep in mind that Ger­many’s first offi­cial case was Jan­u­ary 27. So this new strain was in Ger­many right around the same time the coun­try dis­cov­er its first case. At the same time, with the new evi­dence point­ing towards mil­i­tary ath­letes from France, Spain, and Italy expe­ri­enc­ing COVID-like symp­toms at the Mil­i­tary World Games in Wuhan in late Octo­ber, the ques­tion of when the orig­i­nal strain of the virus first hit Europe is com­plete­ly up in the air at this point.

    Now, as with those pre­vi­ous two stud­ies of this virus based on phy­lo­ge­net­ic analy­sis, this paper has pro­voked a strong back­lash from parts of the virol­o­gy com­mu­ni­ty because the authors spec­u­lat­ed that the this new strain might actu­al­ly be some­how more infec­tious based on its appar­ent abil­i­ty to become the dom­i­nant strain of the virus in an area. Specif­i­cal­ly, the key muta­tion that the authors used to define this new strain, D614G, caus­es an amino acid change in the virus that con­verts an Aspar­tic Acid amino acid (D) to a Glycine (G), which is poten­tial­ly a sig­nif­i­cant change since Aspar­tic Acid is chem­i­cal­ly quite dif­fer­ent from Glycine. And it’s poten­tial­ly even more sig­nif­i­cant because this muta­tion is in the “spike” pro­tein of the virus which is the part of the virus that binds to cells.

    But it also might be a com­plete­ly incon­se­quen­tial muta­tion and the abil­i­ty of the virus­es with that D614G muta­tion to over­take the local strains could be due to ran­dom founder effects. Maybe. We don’t yet know. But we do know that this muta­tion might func­tion­al­ly change the virus and make it more infec­tious which would par­tial­ly explain how it rapid­ly became the dom­i­nant strain in Europe and the US East Coast. And if that’s the case, that also means any ear­li­er strains of this virus that may have been float­ing around Europe or the US in 2019 are almost cer­tain­ly going to be over­tak­en by this new strain, thus obscur­ing the abil­i­ty to ret­ro­spec­tive­ly iden­ti­fy those ear­li­er out­breaks through phy­lo­ge­net­ic analy­ses of iden­ti­fied cas­es.

    But spec­u­la­tion that the new strain is actu­al­ly more infec­tious was­n’t sole­ly based on infer­ence by watch­ing the spread of the strain. The study also includ­ed data from a team at a hos­pi­tal that was treat­ing COVID patients who com­pared the patients that had the old and new strains. The doc­tors found that patients with the new muta­tion had high­er viral loads but there was no dif­fer­ence in hos­pi­tal­iza­tion rates. That’s a dif­fi­cult pair of find­ings to inter­pret but it’s worth recall­ing the recent study that mea­sured the amounts of the virus cre­at­ed by dif­fer­ent strains of the virus in cul­tured human cells and found a wide range of viral load with a 270-fold dif­fer­ence between the slow­est and fastest strains. So if those find­ings in that hos­pi­tal are con­firmed then we might be deal­ing with dif­fer­ent strains that cause very dif­fer­ent lev­els of viral load. And while sim­i­lar hos­pi­tal­iza­tion rates for dif­fer­ent strains with dif­fer­ent viral loads seems coun­ter­in­tu­itive, keep in mind that if that’s actu­al­ly the case and the new strain isn’t more dead­ly than the old­er strain that would make this new strain an effec­tive means of obscur­ing the pres­ence of old­er strains (by inhibit­ing our abil­i­ty to con­duct ret­ro­spec­tive phy­lo­ge­net­ic analy­ses) with­out ulti­mate­ly killing more peo­ple.

    It’s also impor­tant to keep in mind that even if we learn that this virus is mutat­ing in ways that cre­ate real func­tion­al dif­fer­ences in the virus, that’s not an argu­ment against the virus being made in a lab or hav­ing under­gone some sort of pre­vi­ous ‘gain-of-func­tion’ exper­i­ments or direct man­u­al engi­neer­ing. Part of what’s been sur­pris­ing virol­o­gists this whole time as we’ve learned about its struc­ture and func­tion is how it seems like have so many ‘fea­tures’ that make it excep­tion­al­ly good at infect­ing humans. Fea­tures found in the spike pro­tein like the strong propen­si­ty to bind to ACE2 inhibitors, the can­non­i­cal furin cleav­age site, or the abil­i­ty of the virus to infect T‑cells through some alter­na­tive method of enter­ing the cell are all the kinds of fea­tures that did­n’t arise from a sin­gle muta­tion. All of these ‘fea­tures’ could have arisen nat­u­ral­ly over time but the fact that we see of them all in a nov­el virus that we’re told just recent­ly jumped to humans is the remark­able coin­ci­dence that points towards a man-made ori­gin. New muta­tions that arise that might make the virus even more infec­tious don’t some­how dis­count the remark­able num­ber of fea­tures in this virus from the very begin­ning of the out­break that has repeat­ed­ly stunned expe­ri­enced virol­o­gist.

    Now here’s a part of the study that is tru­ly chill­ing if the authors turn out to be cor­rect: the fact that this muta­tion took place on the “spike” pro­tein sug­gests a mech­a­nism through which the virus could rein­fect peo­ple after they recov­er and mutate in ways that requires new ver­sions of a coro­n­avirus vac­cine each year, much like influen­za. And if that’s the case and this virus has the abil­i­ty mutate in ways that thwart vac­cines this is basi­cal­ly a per­ma­nent virus. Will “herd immu­ni­ty” work on a virus that can rein­fect peo­ple and defies vac­cines? We just might find out:

    The Los Ange­les Times

    Sci­en­tists say a now-dom­i­nant strain of the coro­n­avirus appears to be more con­ta­gious than orig­i­nal

    By RALPH VARTABEDIAN
    MAY 5, 2020 4 AM

    Sci­en­tists have iden­ti­fied a new strain of the coro­n­avirus that has become dom­i­nant world­wide and appears to be more con­ta­gious than the ver­sions that spread in the ear­ly days of the COVID-19 pan­dem­ic, accord­ing to a new study led by sci­en­tists at Los Alam­os Nation­al Lab­o­ra­to­ry.

    The new strain appeared in Feb­ru­ary in Europe, migrat­ed quick­ly to the East Coast of the Unit­ed States and has been the dom­i­nant strain across the world since mid-March, the sci­en­tists wrote.

    In addi­tion to spread­ing faster, it may make peo­ple vul­ner­a­ble to a sec­ond infec­tion after a first bout with the dis­ease, the report warned.

    The 33-page report was post­ed Thurs­day on BioRx­iv, a web­site that researchers use to share their work before it is peer reviewed, an effort to speed up col­lab­o­ra­tions with sci­en­tists work­ing on COVID-19 vac­cines or treat­ments. That research has been large­ly based on the genet­ic sequence of ear­li­er strains and might not be effec­tive against the new one.

    The muta­tion iden­ti­fied in the new report affects the now infa­mous spikes on the exte­ri­or of the coro­n­avirus, which allow it to enter human res­pi­ra­to­ry cells. The report’s authors said they felt an “urgent need for an ear­ly warn­ing” so that vac­cines and drugs under devel­op­ment around the world will be effec­tive against the mutat­ed strain.

    Wher­ev­er the new strain appeared, it quick­ly infect­ed far more peo­ple than the ear­li­er strains that came out of Wuhan, Chi­na, and with­in weeks it was the only strain that was preva­lent in some nations, accord­ing to the report. The new strain’s dom­i­nance over its pre­de­ces­sors demon­strates that it is more infec­tious, accord­ing to the report, though exact­ly why is not yet known.

    The coro­n­avirus, known to sci­en­tists as SARS-CoV­‑2, has infect­ed more than 3.5 mil­lion peo­ple around the world and caused more than 250,000 COVID-19 deaths since its dis­cov­ery late last year.

    The report was based on a com­pu­ta­tion­al analy­sis of more than 6,000 coro­n­avirus sequences from around the world, col­lect­ed by the Glob­al Ini­tia­tive for Shar­ing All Influen­za Data, a pub­lic-pri­vate orga­ni­za­tion in Ger­many. Time and again, the analy­sis found the new ver­sion was tran­si­tion­ing to become dom­i­nant.

    The Los Alam­os team, assist­ed by sci­en­tists at Duke Uni­ver­si­ty and the Uni­ver­si­ty of Sheffield in Eng­land, iden­ti­fied 14 muta­tions. Those muta­tions occurred among the near­ly 30,000 base pairs of RNA that oth­er sci­en­tists say make up the coronavirus’s genome. The report authors focused on a muta­tion called D614G, which is respon­si­ble for the change in the virus’ spikes.

    “The sto­ry is wor­ry­ing, as we see a mutat­ed form of the virus very rapid­ly emerg­ing, and over the month of March becom­ing the dom­i­nant pan­dem­ic form,” study leader Bette Kor­ber, a com­pu­ta­tion­al biol­o­gist at Los Alam­os, wrote on her Face­book page. “When virus­es with this muta­tion enter a pop­u­la­tion, they rapid­ly begin to take over the local epi­dem­ic, thus they are more trans­mis­si­ble.”

    ...

    “This is hard news,” wrote Kor­ber, “but please don’t only be dis­heart­ened by it. Our team at LANL was able to doc­u­ment this muta­tion and its impact on trans­mis­sion only because of a mas­sive glob­al effort of clin­i­cal peo­ple and exper­i­men­tal groups, who make new sequences of the virus (SARS-CoV­‑2) in their local com­mu­ni­ties avail­able as quick­ly as they pos­si­bly can.”

    Kor­ber, a grad­u­ate of Cal State Long Beach who went on to earn a PhD in chem­istry at Cal­tech, joined the lab in 1990 and focused much of her work on an HIV vac­cine. In 2004, she won the Ernest Orlan­do Lawrence Award, the U.S. Depart­ment of Energy’s high­est recog­ni­tion for sci­en­tif­ic achieve­ment. She con­tributed a por­tion of the finan­cial prize to help estab­lish an orphan­age for young AIDS vic­tims in South Africa.

    The report con­tains region­al break­downs of when the new strain of virus first emerged and how long it took to become dom­i­nant.

    Italy was one of the first coun­tries to see the new virus in the last week of Feb­ru­ary, almost at the same time that the orig­i­nal strain appeared. Wash­ing­ton was among the first states to get hit with the orig­i­nal strain in late Feb­ru­ary, but by March 15 the mutat­ed strain dom­i­nat­ed. New York was hit by the orig­i­nal virus around March 15, but with­in days the mutant strain took over. The team did not report results for Cal­i­for­nia.

    Sci­en­tists at major orga­ni­za­tions work­ing on a vac­cine or drugs have told The Times that they are pin­ning their hopes on ini­tial evi­dence that the virus is sta­ble and not like­ly to mutate the way influen­za virus does, requir­ing a new vac­cine every year. The Los Alam­os report could upend that assump­tion.

    If the pan­dem­ic fails to wane sea­son­al­ly as the weath­er warms, the study warns, the virus could under­go fur­ther muta­tions even as research orga­ni­za­tions pre­pare the first med­ical treat­ments and vac­cines. With­out get­ting on top of the risk now, the effec­tive­ness of vac­cines could be lim­it­ed. Some of the com­pounds in devel­op­ment are sup­posed to latch onto the spike or inter­rupt its action. If they were designed based on the orig­i­nal ver­sion of the spike, they might not be effec­tive against the new coro­n­avirus strain, the study’s authors warned.

    “We can­not afford to be blind­sided as we move vac­cines and anti­bod­ies into clin­i­cal test­ing,” Kor­ber wrote on Face­book. “Please be encour­aged by know­ing the glob­al sci­en­tif­ic com­mu­ni­ty is on this, and we are coop­er­at­ing with each oth­er in ways I have nev­er seen … in my 30 years as a sci­en­tist.”

    David Mon­te­fiori, a Duke Uni­ver­si­ty sci­en­tist who worked on the report said it is the first to doc­u­ment a muta­tion in the coro­n­avirus that appears to make it more infec­tious.

    Although the researchers don’t yet know the details about how the mutat­ed spike behaves inside the body, it’s clear­ly doing some­thing that gives it an evo­lu­tion­ary advan­tage over its pre­de­ces­sor and is fuel­ing its rapid spread. One sci­en­tist called it a “clas­sic case of Dar­win­ian evo­lu­tion.”

    “D614G is increas­ing in fre­quen­cy at an alarm­ing rate, indi­cat­ing a fit­ness advan­tage rel­a­tive to the orig­i­nal Wuhan strain that enables more rapid spread,” the study said.

    Still unknown is whether this mutant virus could account for region­al vari­a­tions in how hard COVID-19 is hit­ting dif­fer­ent parts of the world.

    In the Unit­ed States, doc­tors had begun to inde­pen­dent­ly ques­tion whether new strains of the virus could account for the dif­fer­ences in how it has infect­ed, sick­ened and killed peo­ple, said Alan Wu, a UC San Fran­cis­co pro­fes­sor who runs the clin­i­cal chem­istry and tox­i­col­o­gy lab­o­ra­to­ries at San Fran­cis­co Gen­er­al Hos­pi­tal.

    Med­ical experts have spec­u­lat­ed in recent weeks that they were see­ing at least two strains of the virus in the U.S., one preva­lent on the East Coast and anoth­er on the West Coast, accord­ing to Wu.

    “We are look­ing to iden­ti­fy the muta­tion,” he said, not­ing that his hos­pi­tal has had only a few deaths out of the hun­dreds of cas­es it has treat­ed, which is “quite a dif­fer­ent sto­ry than we are hear­ing from New York.”

    The Los Alam­os study does not indi­cate that the new ver­sion of the virus is more lethal than the orig­i­nal. Peo­ple infect­ed with the mutat­ed strain appear to have high­er viral loads. But the study’s authors from the Uni­ver­si­ty of Sheffield found that among a local sam­ple of 447 patients, hos­pi­tal­iza­tion rates were about the same for peo­ple infect­ed with either virus ver­sion.

    Even if the new strain is no more dan­ger­ous than the oth­ers, it could still com­pli­cate efforts to bring the pan­dem­ic under con­trol. That would be an issue if the muta­tion makes the virus so dif­fer­ent from ear­li­er strains that peo­ple who have immu­ni­ty to them would not be immune to the new ver­sion.

    If that is indeed the case, it could make “indi­vid­u­als sus­cep­ti­ble to a sec­ond infec­tion,” the study authors wrote.

    It’s pos­si­ble that the muta­tion changes the spike in some way that helps the virus evade the immune sys­tem, said Mon­te­fiori, who has worked on an HIV vac­cine for 30 years. “It is hypo­thet­i­cal. We are look­ing at it very hard.”

    ———–

    “Sci­en­tists say a now-dom­i­nant strain of the coro­n­avirus appears to be more con­ta­gious than orig­i­nal” by RALPH VARTABEDIAN; The Los Ange­les Times; 05/05/2020

    “The muta­tion iden­ti­fied in the new report affects the now infa­mous spikes on the exte­ri­or of the coro­n­avirus, which allow it to enter human res­pi­ra­to­ry cells. The report’s authors said they felt an “urgent need for an ear­ly warn­ing” so that vac­cines and drugs under devel­op­ment around the world will be effec­tive against the mutat­ed strain.”

    Yep, it’s not just a ran­dom muta­tion. It’s a spike pro­tein muta­tion. That’s a bad place for a muta­tion on this virus. And in this case, the mutant strain was found to become the preva­lent strain in some nations with­in weeks. They report see­ing this pat­tern over and over:

    ...
    Wher­ev­er the new strain appeared, it quick­ly infect­ed far more peo­ple than the ear­li­er strains that came out of Wuhan, Chi­na, and with­in weeks it was the only strain that was preva­lent in some nations, accord­ing to the report. The new strain’s dom­i­nance over its pre­de­ces­sors demon­strates that it is more infec­tious, accord­ing to the report, though exact­ly why is not yet known.

    ...

    The report was based on a com­pu­ta­tion­al analy­sis of more than 6,000 coro­n­avirus sequences from around the world, col­lect­ed by the Glob­al Ini­tia­tive for Shar­ing All Influen­za Data, a pub­lic-pri­vate orga­ni­za­tion in Ger­many. Time and again, the analy­sis found the new ver­sion was tran­si­tion­ing to become dom­i­nant.

    The Los Alam­os team, assist­ed by sci­en­tists at Duke Uni­ver­si­ty and the Uni­ver­si­ty of Sheffield in Eng­land, iden­ti­fied 14 muta­tions. Those muta­tions occurred among the near­ly 30,000 base pairs of RNA that oth­er sci­en­tists say make up the coronavirus’s genome. The report authors focused on a muta­tion called D614G, which is respon­si­ble for the change in the virus’ spikes.

    “The sto­ry is wor­ry­ing, as we see a mutat­ed form of the virus very rapid­ly emerg­ing, and over the month of March becom­ing the dom­i­nant pan­dem­ic form,” study leader Bette Kor­ber, a com­pu­ta­tion­al biol­o­gist at Los Alam­os, wrote on her Face­book page. “When virus­es with this muta­tion enter a pop­u­la­tion, they rapid­ly begin to take over the local epi­dem­ic, thus they are more trans­mis­si­ble.”
    ...

    And it’s those repeat­ed obser­va­tions that this strain over­took the old­er strain in coun­try after coun­try com­bined with the fact that the muta­tion is in the spike pro­tein that led the researchers to spec­u­late that the muta­tion real­ly did some­how make this new strain more infec­tious. And if that’s true, it’s the kind of find­ing that serves as an omi­nous warn­ing that vac­cines real­ly might not be as effec­tive as we hope for because it’s the spike pro­tein that vac­cines are going to tar­get. In addi­tion, muta­tions in the spike pro­tein might explain why some peo­ple appear to get rein­fect­ed. Is herd immu­ni­ty pos­si­ble for a virus that can rein­fect peo­ple?

    ...
    Sci­en­tists at major orga­ni­za­tions work­ing on a vac­cine or drugs have told The Times that they are pin­ning their hopes on ini­tial evi­dence that the virus is sta­ble and not like­ly to mutate the way influen­za virus does, requir­ing a new vac­cine every year. The Los Alam­os report could upend that assump­tion.

    If the pan­dem­ic fails to wane sea­son­al­ly as the weath­er warms, the study warns, the virus could under­go fur­ther muta­tions even as research orga­ni­za­tions pre­pare the first med­ical treat­ments and vac­cines. With­out get­ting on top of the risk now, the effec­tive­ness of vac­cines could be lim­it­ed. Some of the com­pounds in devel­op­ment are sup­posed to latch onto the spike or inter­rupt its action. If they were designed based on the orig­i­nal ver­sion of the spike, they might not be effec­tive against the new coro­n­avirus strain, the study’s authors warned.

    ...

    “D614G is increas­ing in fre­quen­cy at an alarm­ing rate, indi­cat­ing a fit­ness advan­tage rel­a­tive to the orig­i­nal Wuhan strain that enables more rapid spread,” the study said.

    ...

    Even if the new strain is no more dan­ger­ous than the oth­ers, it could still com­pli­cate efforts to bring the pan­dem­ic under con­trol. That would be an issue if the muta­tion makes the virus so dif­fer­ent from ear­li­er strains that peo­ple who have immu­ni­ty to them would not be immune to the new ver­sion.

    If that is indeed the case, it could make “indi­vid­u­als sus­cep­ti­ble to a sec­ond infec­tion,” the study authors wrote.

    It’s pos­si­ble that the muta­tion changes the spike in some way that helps the virus evade the immune sys­tem, said Mon­te­fiori, who has worked on an HIV vac­cine for 30 years. “It is hypo­thet­i­cal. We are look­ing at it very hard.”
    ...

    Adding to the omi­nous­ness is the fact that the study includ­ed a com­par­i­son of patients with the old­er and new strains and the patients with the new strain appear to have a high­er viral load. And yet they weren’t hos­pi­tal­ized at the same rate. It’s the kind of coun­ter­in­tu­itive find­ing that, if accu­rate, under­scores how lit­tle we under­stand about this virus at this point:

    ...

    Med­ical experts have spec­u­lat­ed in recent weeks that they were see­ing at least two strains of the virus in the U.S., one preva­lent on the East Coast and anoth­er on the West Coast, accord­ing to Wu.

    “We are look­ing to iden­ti­fy the muta­tion,” he said, not­ing that his hos­pi­tal has had only a few deaths out of the hun­dreds of cas­es it has treat­ed, which is “quite a dif­fer­ent sto­ry than we are hear­ing from New York.”

    The Los Alam­os study does not indi­cate that the new ver­sion of the virus is more lethal than the orig­i­nal. Peo­ple infect­ed with the mutat­ed strain appear to have high­er viral loads. But the study’s authors from the Uni­ver­si­ty of Sheffield found that among a local sam­ple of 447 patients, hos­pi­tal­iza­tion rates were about the same for peo­ple infect­ed with either virus ver­sion.
    ...

    Ok, now let’s quick­ly look at an excerpt from the actu­al paper itself where they go into more detail on where they observed the first sam­ples of the new “G” form of the virus. The ear­li­est Euro­pean sam­ple was found in Ger­many on 1/28/2020. There were four sam­ples found in Chi­na: one Zhe­jiang on 1/24/2020, two from Shang­hai on 1/28/2020 and 2/6/2020, and one from Wuhan on 2/7/2020. Keep in mind that we are lim­it­ed to the sam­pled data so while sam­ple in Zhe­jiang was found 4 days ear­li­er than the one in Ger­many we have no idea which of those infec­tions actu­al­ly came first:

    bioRx­iv

    Spike muta­tion pipeline reveals the emer­gence of a more trans­mis­si­ble form of SARS-CoV­‑2

    Kor­ber B, Fis­ch­er WM, Gnanakaran S, Yoon H, Theil­er J, Abfal­ter­er W, Foley B, Gior­gi EE, Bhat­tacharya T,Parker MD, Par­tridge DG, Evans CM, de Sil­va TI, on behalf of the Sheffield COVID-19 Genomics Group, LaBrancheCC, and Mon­te­fior­iDC

    post­ed April 30, 2020

    ...

    The D614G muta­tion

    Increas­ing fre­quen­cy and glob­al dis­tri­b­u­tion. The muta­tion D614G (a G‑to‑A base change at posi­tion 23,403 in the Wuhan ref­er­ence strain) was the only site of inter­est iden­ti­fied in our first Spike muta­tion report in ear­ly March (Fig. 1A); it was found 7 times in 183 sequences that were avail­able at the time. Four of these sev­en first D614G strains were sam­pled in Europe, and one each in Mex­i­co, Brazil, and in Wuhan. In 5/7 cas­es, D614G was accom­pa­nied by 2 oth­er muta­tions: a silent C‑to‑T muta­tion in the nsp3 gene at posi­tion 3,037, and a C‑to‑T muta­tion at posi­tion 14,409 which results ina RNA-depen­dent RNA poly­merase (RdRp) amino acid change (RdRp P323L). The com­bi­na­tion of these three muta­tions forms the basis for the clade that soon emerged in Europe (Fig. 1). By the time of our sec­ond report in mid-March, D614G was being tracked at the GISAID due to its high fre­quen­cy, and referred to as the “G” clade; it was present in 29% of the glob­al sam­ples, but was still found almost exclu­sive­ly in Europe. It was recent­ly report­ed by Pachet­ti et al.to be found in Europe and absent from regions glob­al­ly, pre­sum­ably because they cap­ture GISAID data in rough­ly the time frame as our sec­ond report (Pachet­ti et al., 2020). The data avail­able for study mid-March, giv­en an approx­i­mate 2‑week lag time between sam­pling and report­ing, were con­sis­tent with the pos­si­bil­i­ty of a founder effect in Europe result­ing in spread across the con­ti­nent, cou­pled with an increase in Euro­pean sam­pling in the data­base. How­ev­er, an ear­ly April sam­pling of the data from GISAID showed that G614’s fre­quen­cy was increas­ing at an alarm­ing pace through­out March, and it was clear­ly show­ing an ever-broad­en­ing geo­graph­ic spread(Fig. 1A).

    To dif­fer­en­ti­ate between founder effects and a selec­tive advan­tage dri­ving the increas­ing fre­quen­cy of the G clade in the GISAID data, we applied the suite of tools that we had been devel­op­ing for the SARS-CoV­‑2 analy­sis pipeline (Fig. 2, Fig. 3, Fig. S2 and Fig. S3). A clear and con­sis­tent pat­tern was observed in almost every place where ade­quate sam­pling was avail­able. In most coun­tries and states where the COVID-19 epi­dem­ic was ini­ti­at­ed and where sequences were sam­pled pri­or to March 1, the D614 form was the dom­i­nant local form ear­ly in the epi­dem­ic (orange in Figs. 2 and 3). Wher­ev­er G614 entered a pop­u­la­tion, a rapid rise inits fre­quen­cy fol­lowed, and in many cas­es G614 became the dom­i­nant local form in a mat­ter of only a few weeks (Fig. 3 and S3).

    In Europe, where the G614 first began its expan­sion, the D614 and G614 forms were co-cir­cu­lat­ing ear­ly in the epi­dem­ic, with D614 more com­mon in most sam­pled coun­tries, the excep­tions being Italy and Switzer­land (Fig. 2A). Through March, G614 became increas­ing­ly com­mon through­out Europe, and by April it dom­i­nat­ed con­tem­po­rary sam­pling (Fig. 2 and 3). In North Amer­i­ca, infec­tions were ini­ti­at­ed and estab­lished across the con­ti­nent by the orig­i­nal D614 form, but in ear­ly March, the G614 was intro­duced into both Cana­da and the USA, and by the end of March it had become the dom­i­nant form in both nations. Wash­ing­ton state, the state with the great­est num­ber of avail­able GISAID SARS-CoV­‑2 sequences from the USA, exem­pli­fies this pat­tern (Fig­ure 3 and S3), and a sim­i­lar shift over time is evi­dent in many oth­er states with sam­ples avail­able through­out March (detailed data by state pro­vid­ed in Item S2). Sequences from New York were poor­ly sam­pled until some days into March(Fig. 3),and the G614 form was the pre­dom­i­nant form; the G614 form was com­ing into promi­nence else­where in the USA by that time. Thus it is not clear whether the local pan­dem­ic was seed­ed by Euro­pean con­tacts, as sug­gest­ed in(Brufsky, 2020), if it was seed­ed by con­tacts from with­in the USA where it had already achieved high preva­lence, or by a com­bi­na­tion of both routes. Aus­tralia fol­lows the same tran­si­tion pat­tern, from D614 to G614 dom­i­nance, as the USA and Cana­da. Ice­land is the sin­gle excep­tion to the pat­tern; there sequenc­ing was exten­sive and the epi­dem­ic seems to have start­ed with a G614 form, but there was a tran­sient increase in the D614 form, which then per­sist­ed at con­stant low lev­el (Fig. 3 and S3). Asian sam­ples were com­plete­ly dom­i­nat­ed by the orig­i­nal Wuhan D614 form through mid-March, but by mid-March in Asian coun­tries out­side of Chi­na, the G614 form was clear­ly estab­lished and expand­ing (Figs 2 and 3). The sta­tus of the D614G muta­tion in Chi­na remains unclear, as very few Chi­nese sequences in GISAID were sam­pled after March 1. South Amer­i­ca and Africa remain sparse­ly sam­pled, but are shown for com­plete­ness in Figs. 2 and 3; for details see Item S2. Tak­en togeth­er, the data shows that G614 con­fers a selec­tive advan­tage that is repeat­ed­ly reflect­ed by dra­mat­ic shifts to G614 forms in region­al epi­demics over a peri­od of sev­er­al weeks.

    The ear­li­est D614G muta­tion in Europe was iden­ti­fied in Ger­many (EPI_ISL_406862, sam­pled 1/28/2020), and it was accom­pa­nied by the C‑to‑T muta­tion at 3,037, but not by the muta­tion at 14,409. Of poten­tial inter­est for under­stand­ing the ori­gin of the G614 clade, the G614 form of the virus was also found 4 times in Chi­na among ear­ly samples(Item S2). A Wuhan sequence (EPI_ISL_412982) sam­pled on 2/7/2020 had the D614G muta­tion, but it did not have either of the two accom­pa­ny­ing muta­tions, and this sin­gle D614G muta­tion may have arisen inde­pen­dent­ly (Fig. 1). The oth­er three cas­es were poten­tial­ly relat­ed to the Ger­man sequence. One sequence sam­pled on 1/24/2020 was from Zhe­jiang (EPI_ISL_422425), which bor­ders Shang­hai, and it had all three muta­tions asso­ci­at­ed with the G clade that expand­ed in Europe. The oth­er two sam­ples were both from Shang­hai, and sam­pled on 1/28/2020 and 2/6/2020 (EPI_ISL_416327, EPI_ISL_416334); like the Ger­man sequence they lacked the muta­tion­at 14,409. Giv­en that these ear­ly Chi­nese sequences were also high­ly relat­ed to the Ger­man sequence through­out their genomes, it is pos­si­ble that the G614 may have orig­i­nat­ed either in Chi­na or in Europe as it was present in both places in late Jan­u­ary. There are no recent GISAID sequences from Shang­hai or Zhe­jian­gat this time, so we do not know if G614 was pref­er­en­tial­ly trans­mit­ted there, but the D614 form was preva­lent in Shang­hai in Jan­u­ary and ear­ly Feb­ru­ary.

    ...

    ———–


    Spike muta­tion­pipelinere­veals the emer­gence of a more trans­mis­si­ble for­mof SARS-CoV­‑2″ by Kor­ber et al.; bioRx­iv; 04/30/2020

    “...Giv­en that these ear­ly Chi­nese sequences were also high­ly relat­ed to the Ger­man sequence through­out their genomes, it is pos­si­ble that the G614 may have orig­i­nat­ed either in Chi­na or in Europe as it was present in both places in late Jan­u­ary.”

    That’s the best guess we have at this point in terms of where this strain orig­i­nat­ed: it could have been Chi­na or Europe because it appeared to sud­den­ly be present in both places in the last week of Jan­u­ary. But regard­less of where this new strain emerged, the observed fact is that it appears to over­take the local strains when it moves into an area would make allow­ing the spread of this virus quite tempt­ing of there was a desire to obscure an ear­li­er out­break by allow­ing the new­er strain to move into loca­tions where old­er strains may have been qui­et­ly float­ing around and mak­ing it like­ly that the new­er strain is what gets sam­pled, sequenced, and uploaded to the GISAID data­base. Espe­cial­ly if the sam­pling takes place belat­ed­ly because the Pres­i­dent is under­cut­ting the util­i­ty of test­ing and push­ing for the pre­ma­ture reopen­ing of the econ­o­my no mat­ter what.

    Now, regard­ing the warn­ings about the com­pli­ca­tions on devel­op­ing vac­cines, how big of a com­pli­ca­tion might it be? One sce­nario is some­thing like influen­za, where a new ver­sion of the vac­cine needs to be devel­oped each year in the hope of antic­i­pat­ing what the new glob­al strain will look like. But as the fol­low­ing arti­cle points out, there’s a far more dire pos­si­bil­i­ty and it’s not at all unimag­in­able because it’s a sce­nario we’ve seen before: Maybe we’ll nev­er devel­op a vac­cine, like what hap­pened with HIV:

    CNN

    What hap­pens if a coro­n­avirus vac­cine is nev­er devel­oped? It has hap­pened before

    By Rob Picheta, CNN
    Updat­ed 12:59 PM ET, Sun May 3, 2020

    Lon­don (CNN)As coun­tries lie frozen in lock­down and bil­lions of peo­ple lose their liveli­hoods, pub­lic fig­ures are teas­ing a break­through that would mark the end of the crip­pling coro­n­avirus pan­dem­ic: a vac­cine.

    But there is anoth­er, worst-case pos­si­bil­i­ty: that no vac­cine is ever devel­oped. In this out­come, the pub­lic’s hopes are repeat­ed­ly raised and then dashed, as var­i­ous pro­posed solu­tions fall before the final hur­dle.

    Instead of wip­ing out Covid-19, soci­eties may instead learn to live with it. Cities would slow­ly open and some free­doms will be returned, but on a short leash, if experts’ rec­om­men­da­tions are fol­lowed. Test­ing and phys­i­cal trac­ing will become part of our lives in the short term, but in many coun­tries, an abrupt instruc­tion to self-iso­late could come at any time. Treat­ments may be devel­oped — but out­breaks of the dis­ease could still occur each year, and the glob­al death toll would con­tin­ue to tick upwards.

    It’s a path rarely pub­licly coun­te­nanced by politi­cians, who are speak­ing opti­misti­cal­ly about human tri­als already under­way to find a vac­cine. But the pos­si­bil­i­ty is tak­en very seri­ous­ly by many experts — because it’s hap­pened before. Sev­er­al times.

    “There are some virus­es that we still do not have vac­cines against,” says Dr. David Nabar­ro, a pro­fes­sor of glob­al health at Impe­r­i­al Col­lege Lon­don, who also serves as a spe­cial envoy to the World Health Orga­ni­za­tion on Covid-19. “We can’t make an absolute assump­tion that a vac­cine will appear at all, or if it does appear, whether it will pass all the tests of effi­ca­cy and safe­ty.

    “It’s absolute­ly essen­tial that all soci­eties every­where get them­selves into a posi­tion where they are able to defend against the coro­n­avirus as a con­stant threat, and to be able to go about social life and eco­nom­ic activ­i­ty with the virus in our midst,” Nabar­ro tells CNN.

    Most experts remain con­fi­dent that a Covid-19 vac­cine will even­tu­al­ly be devel­oped; in part because, unlike pre­vi­ous dis­eases like HIV and malar­ia, the coro­n­avirus does not mutate rapid­ly.

    Many, includ­ing Nation­al Insti­tute of Aller­gy and Infec­tious Dis­eases direc­tor Dr. Antho­ny Fau­ci, sug­gest it could hap­pen in a year to 18 months. Oth­er fig­ures, like Eng­land’s Chief Med­ical Offi­cer Chris Whit­ty, have veered towards the more dis­tant end of the spec­trum, sug­gest­ing that a year may be too soon.

    But even if a vac­cine is devel­oped, bring­ing it to fruition in any of those time­frames would be a feat nev­er achieved before.

    “We’ve nev­er accel­er­at­ed a vac­cine in a year to 18 months,” Dr. Peter Hotez, dean of the Nation­al School of Trop­i­cal Med­i­cine at Bay­lor Col­lege of Med­i­cine in Hous­ton, tells CNN. “It does­n’t mean it’s impos­si­ble, but it will be quite a hero­ic achieve­ment.

    “We need plan A, and a plan B,” he says.

    When vac­cines don’t work

    In 1984, the US Sec­re­tary of Health and Human Ser­vices Mar­garet Heck­ler announced at a press con­fer­ence in Wash­ing­ton, DC, that sci­en­tists had suc­cess­ful­ly iden­ti­fied the virus that lat­er became known as HIV — and pre­dict­ed that a pre­ven­ta­tive vac­cine would be ready for test­ing in two years.

    Near­ly four decades and 32 mil­lion deaths lat­er, the world is still wait­ing for an HIV vac­cine.

    Instead of a break­through, Heck­ler’s claim was fol­lowed by the loss of much of a gen­er­a­tion of gay men and the painful shun­ning of their com­mu­ni­ty in West­ern coun­tries. For many years, a pos­i­tive diag­no­sis was not only a death sen­tence; it ensured a per­son would spend their final months aban­doned by their com­mu­ni­ties, while doc­tors debat­ed in med­ical jour­nals whether HIV patients were even worth sav­ing.

    The search did­n’t end in the 1980s. In 1997, Pres­i­dent Bill Clin­ton chal­lenged the US to come up with a vac­cine with­in a decade. Four­teen years ago, sci­en­tists said we were still about 10 years away.

    The dif­fi­cul­ties in find­ing a vac­cine began with the very nature of HIV/AIDS itself. “Influen­za is able to change itself from one year to the next so the nat­ur­al infec­tion or immu­niza­tion the pre­vi­ous year does­n’t infect you the fol­low­ing year. HIV does that dur­ing a sin­gle infec­tion,” explains Paul Offit, a pedi­a­tri­cian and infec­tious dis­ease spe­cial­ist who co-invent­ed the rotavirus vac­cine.

    “It con­tin­ues to mutate in you, so it’s like you’re infect­ed with a thou­sand dif­fer­ent HIV strands,” Offit tells CNN. “(And) while it is mutat­ing, it’s also crip­pling your immune sys­tem.”

    HIV pos­es very unique dif­fi­cul­ties and Covid-19 does not pos­sess its lev­el of elu­sive­ness, mak­ing experts gen­er­al­ly more opti­mistic about find­ing a vac­cine.

    But there have been oth­er dis­eases that have con­found­ed both sci­en­tists and the human body. An effec­tive vac­cine for dengue fever, which infects as many as 400,000 peo­ple a year accord­ing to the WHO, has elud­ed doc­tors for decades. In 2017, a large-scale effort to find one was sus­pend­ed after it was found to wors­en the symp­toms of the dis­ease.

    Sim­i­lar­ly, it’s been very dif­fi­cult to devel­op vac­cines for the com­mon rhi­novirus­es and ade­n­ovirus­es — which, like coro­n­avirus­es, can cause cold symp­toms. There’s just one vac­cine to pre­vent two strains of ade­n­ovirus, and it’s not com­mer­cial­ly avail­able.

    “You have high hopes, and then your hopes are dashed,” says Nabar­ro, describ­ing the slow and painful process of devel­op­ing a vac­cine. “We’re deal­ing with bio­log­i­cal sys­tems, we’re not deal­ing with mechan­i­cal sys­tems. It real­ly depends so much on how the body reacts.”

    Human tri­als are already under­way at Oxford Uni­ver­si­ty in Eng­land for a coro­n­avirus vac­cine made from a chim­panzee virus, and in the US for a dif­fer­ent vac­cine, pro­duced by Mod­er­na.

    How­ev­er, it is the test­ing process — not the devel­op­ment — that holds up and often scup­pers the pro­duc­tion of vac­cines, adds Hotez, who worked on a vac­cine to pro­tect against SARS. “The hard part is show­ing you can prove that it works and it’s safe.”

    Plan B

    If the same fate befalls a Covid-19 vac­cine, the virus could remain with us for many years. But the med­ical response to HIV/AIDS still pro­vides a frame­work for liv­ing with a dis­ease we can’t stamp out.

    “In HIV, we’ve been able to make that a chron­ic dis­ease with antivi­rals. We’ve done what we’ve always hoped to do with can­cer,” Offit says. “It’s not the death sen­tence it was in the 1980s.”

    ...

    But how effec­tive a treat­ment is would depend on which one works — remde­sivir is not in high sup­ply inter­na­tion­al­ly and scal­ing up its pro­duc­tion would cause prob­lems.

    And cru­cial­ly, any treat­ment won’t pre­vent infec­tions occur­ring in soci­ety — mean­ing the coro­n­avirus would be eas­i­er to man­age and the pan­dem­ic would sub­side, but the dis­ease could be with us many years into the future.

    What life with­out a vac­cine looks like

    If a vac­cine can’t be pro­duced, life will not remain as it is now. It just might not go back to nor­mal quick­ly.

    “The lock­down is not sus­tain­able eco­nom­i­cal­ly, and pos­si­bly not polit­i­cal­ly,” says Neal. “So we need oth­er things to con­trol it.”

    That means that, as coun­tries start to creep out of their paral­y­ses, experts would push gov­ern­ments to imple­ment an awk­ward new way of liv­ing and inter­act­ing to buy the world time in the months, years or decades until Covid-19 can be elim­i­nat­ed by a vac­cine.

    “It is absolute­ly essen­tial to work on being Covid-ready,” Nabar­ro says. He calls for a new “social con­tract” in which cit­i­zens in every coun­try, while start­ing to go about their nor­mal lives, take per­son­al respon­si­bil­i­ty to self-iso­late if they show symp­toms or come into con­tact with a poten­tial Covid-19 case.

    It means the cul­ture of shrug­ging off a cough or light cold symp­toms and trudg­ing into work should be over. Experts also pre­dict a per­ma­nent change in atti­tudes towards remote work­ing, with work­ing from home, at least on some days, becom­ing a stan­dard way of life for white col­lar employ­ees. Com­pa­nies would be expect­ed to shift their rotas so that offices are nev­er full unnec­es­sar­i­ly.

    “It (must) become a way of behav­ing that we all ascribe to per­son­al respon­si­bil­i­ty ... treat­ing those who are iso­lat­ed as heroes rather than pari­ahs,” says Nabar­ro. “A col­lec­tive pact for sur­vival and well-being in the face of the threat of the virus.

    “It’s going to be dif­fi­cult to do in poor­er nations,” he adds, so find­ing ways to sup­port devel­op­ing coun­tries will become “par­tic­u­lar­ly polit­i­cal­ly tricky, but also very impor­tant.” He cites tight­ly packed refugee and migrant set­tle­ments as areas of espe­cial­ly high con­cern.

    In the short term, Nabar­ro says a vast pro­gram of test­ing and con­tact trac­ing would need to be imple­ment­ed to allow life to func­tion along­side Covid-19 — one which dwarfs any such pro­gram ever estab­lished to fight an out­break, and which remains some time away in major coun­tries like the US and the UK.

    “Absolute­ly crit­i­cal is going to be hav­ing a pub­lic health sys­tem in place that includes con­tact trac­ing, diag­no­sis in the work­place, mon­i­tor­ing for syn­dromic sur­veil­lance, ear­ly com­mu­ni­ca­tion on whether we have to re-imple­ment social dis­tanc­ing,” adds Hotez. “It’s doable, but it’s com­pli­cat­ed and we real­ly haven’t done it before.”

    Those sys­tems could allow for some social inter­ac­tions to return. “If there’s min­i­mal trans­mis­sion, it may indeed be pos­si­ble to open things up for sport­ing events” and oth­er large gath­er­ings, says Hotez — but such a move would not be per­ma­nent and would con­tin­u­al­ly be assessed by gov­ern­ments and pub­lic health bod­ies.

    That means the the Pre­mier League, NFL and oth­er mass events could go ahead with their sched­ules as long as ath­letes are get­ting reg­u­lar­ly test­ed, and wel­come in fans for weeks at a time — per­haps sep­a­rat­ed with­in the stands — before quick­ly shut­ting sta­di­ums if the threat ris­es.

    “Bars and pubs are prob­a­bly last on the list as well, because they are over­crowd­ed,” sug­gests Neal. “They could reopen as restau­rants, with social dis­tanc­ing.” Some Euro­pean coun­tries have sig­naled they will start allow­ing restau­rants to serve cus­tomers at vast­ly reduced capac­i­ty.

    Restric­tions are most like­ly to come back over the win­ter, with Hotez sug­gest­ing that Covid-19 peaks could occur every win­ter until a vac­cine is intro­duced.

    And lock­downs, many of which are in the process of grad­u­al­ly being lift­ed, could return at any moment. “From time to time there will be out­breaks, move­ment will be restrict­ed — and that may apply to parts of a coun­try, or it may even apply to a whole coun­try,” Nabar­ro says.

    The more time pass­es, the more impos­ing becomes the hot­ly debat­ed prospect of herd immu­ni­ty — reached when the major­i­ty of a giv­en pop­u­la­tion, around 70% to 90%, becomes immune to an infec­tious dis­ease. “That does to some extent lim­it spread,” Offit says — “although pop­u­la­tion immu­ni­ty caused by nat­ur­al infec­tion is not the best way to pro­vide pop­u­la­tion immu­ni­ty. The best way is with a vac­cine.”

    Measles is the “per­fect exam­ple,” says Offit — before vac­cines became wide­spread, “every year 2 to 3 mil­lion peo­ple would get measles, and that would be true here too.” In oth­er words, the amount of death and suf­fer­ing from Covid-19 would be vast even if a large por­tion of the pop­u­la­tion is not sus­cep­ti­ble.

    All of these pre­dic­tions are tem­pered by a gen­er­al belief that a vac­cine will, even­tu­al­ly, be devel­oped. “I do think there’ll be vac­cine — there’s plen­ty of mon­ey, there’s plen­ty of inter­est and the tar­get is clear,” Offit says.

    But if pre­vi­ous out­breaks have proven any­thing, it’s that hunts for vac­cines are unpre­dictable. “I don’t think any vac­cine has been devel­oped quick­ly,” Offit cau­tions. “I’d be real­ly amazed if we had some­thing in 18 months.”

    ———-

    “What hap­pens if a coro­n­avirus vac­cine is nev­er devel­oped? It has hap­pened before” by Rob Picheta; CNN; 05/03/2020

    But there is anoth­er, worst-case pos­si­bil­i­ty: that no vac­cine is ever devel­oped. In this out­come, the pub­lic’s hopes are repeat­ed­ly raised and then dashed, as var­i­ous pro­posed solu­tions fall before the final hur­dle.”

    Are we in store for decades of annu­al COVID out­breaks? The answer appears to be a defin­i­tive ‘maybe’. We have no idea at this point in part because our expe­ri­ence on these mat­ters is so mixed. But if that worst-case sce­nario pans out, we could be look­ing at decades where hyper-vig­i­lance is the only option oth­er than just let­ting the pan­dem­ic run ram­pant and sys­tem­at­i­cal­ly kill off the vul­ner­a­ble each year. An ever present virus ready to kill off the elder­ly and immuno­log­i­cal­ly vul­ner­a­ble. Refugees crammed into camps would be par­tic­u­lar­ly vul­ner­a­ble:

    ...
    Instead of wip­ing out Covid-19, soci­eties may instead learn to live with it. Cities would slow­ly open and some free­doms will be returned, but on a short leash, if experts’ rec­om­men­da­tions are fol­lowed. Test­ing and phys­i­cal trac­ing will become part of our lives in the short term, but in many coun­tries, an abrupt instruc­tion to self-iso­late could come at any time. Treat­ments may be devel­oped — but out­breaks of the dis­ease could still occur each year, and the glob­al death toll would con­tin­ue to tick upwards.

    It’s a path rarely pub­licly coun­te­nanced by politi­cians, who are speak­ing opti­misti­cal­ly about human tri­als already under­way to find a vac­cine. But the pos­si­bil­i­ty is tak­en very seri­ous­ly by many experts — because it’s hap­pened before. Sev­er­al times.

    “There are some virus­es that we still do not have vac­cines against,” says Dr. David Nabar­ro, a pro­fes­sor of glob­al health at Impe­r­i­al Col­lege Lon­don, who also serves as a spe­cial envoy to the World Health Orga­ni­za­tion on Covid-19. “We can’t make an absolute assump­tion that a vac­cine will appear at all, or if it does appear, whether it will pass all the tests of effi­ca­cy and safe­ty.

    “It’s absolute­ly essen­tial that all soci­eties every­where get them­selves into a posi­tion where they are able to defend against the coro­n­avirus as a con­stant threat, and to be able to go about social life and eco­nom­ic activ­i­ty with the virus in our midst,” Nabar­ro tells CNN.

    ...

    “It (must) become a way of behav­ing that we all ascribe to per­son­al respon­si­bil­i­ty ... treat­ing those who are iso­lat­ed as heroes rather than pari­ahs,” says Nabar­ro. “A col­lec­tive pact for sur­vival and well-being in the face of the threat of the virus.

    “It’s going to be dif­fi­cult to do in poor­er nations,” he adds, so find­ing ways to sup­port devel­op­ing coun­tries will become “par­tic­u­lar­ly polit­i­cal­ly tricky, but also very impor­tant.” He cites tight­ly packed refugee and migrant set­tle­ments as areas of espe­cial­ly high con­cern.
    ...

    And that’s assum­ing that the virus behaves like influen­za. Let’s hope it’s only that and you only get infect­ed with one strain at a time. What if it’s like HIV, where once you get infect­ed new strains can start emerg­ing in your own body? Now, as of now it does­n’t look like the virus can just go dor­mant in the body like HIV (although there have been fears that it can) which would encour­age the devel­op­ment of new strains in the body, but we’re still learn­ing about it. And if this becomes a per­ma­nent glob­al pan­dem­ic that’s going to give the virus a lot of oppor­tu­ni­ties to devel­op new ‘fea­tures’ like that:

    ...
    The dif­fi­cul­ties in find­ing a vac­cine began with the very nature of HIV/AIDS itself. “Influen­za is able to change itself from one year to the next so the nat­ur­al infec­tion or immu­niza­tion the pre­vi­ous year does­n’t infect you the fol­low­ing year. HIV does that dur­ing a sin­gle infec­tion,” explains Paul Offit, a pedi­a­tri­cian and infec­tious dis­ease spe­cial­ist who co-invent­ed the rotavirus vac­cine.

    “It con­tin­ues to mutate in you, so it’s like you’re infect­ed with a thou­sand dif­fer­ent HIV strands,” Offit tells CNN. “(And) while it is mutat­ing, it’s also crip­pling your immune sys­tem.”

    HIV pos­es very unique dif­fi­cul­ties and Covid-19 does not pos­sess its lev­el of elu­sive­ness, mak­ing experts gen­er­al­ly more opti­mistic about find­ing a vac­cine.

    But there have been oth­er dis­eases that have con­found­ed both sci­en­tists and the human body. An effec­tive vac­cine for dengue fever, which infects as many as 400,000 peo­ple a year accord­ing to the WHO, has elud­ed doc­tors for decades. In 2017, a large-scale effort to find one was sus­pend­ed after it was found to wors­en the symp­toms of the dis­ease.

    Sim­i­lar­ly, it’s been very dif­fi­cult to devel­op vac­cines for the com­mon rhi­novirus­es and ade­n­ovirus­es — which, like coro­n­avirus­es, can cause cold symp­toms. There’s just one vac­cine to pre­vent two strains of ade­n­ovirus, and it’s not com­mer­cial­ly avail­able.
    ...

    But if HIV isn’t the best anal­o­gy for what to expect if this virus does end up being resis­tant to vac­cine, per­haps a bet­ter exam­ple is the measles. A hyper­in­fec­tious dis­ease that would rou­tine­ly kill mil­lions a year until we devel­oped a vac­cine. Even with “herd immu­ni­ty”, measles still killed mil­lions:

    ...
    The more time pass­es, the more impos­ing becomes the hot­ly debat­ed prospect of herd immu­ni­ty — reached when the major­i­ty of a giv­en pop­u­la­tion, around 70% to 90%, becomes immune to an infec­tious dis­ease. “That does to some extent lim­it spread,” Offit says — “although pop­u­la­tion immu­ni­ty caused by nat­ur­al infec­tion is not the best way to pro­vide pop­u­la­tion immu­ni­ty. The best way is with a vac­cine.”

    Measles is the “per­fect exam­ple,” says Offit — before vac­cines became wide­spread, “every year 2 to 3 mil­lion peo­ple would get measles, and that would be true here too.” In oth­er words, the amount of death and suf­fer­ing from Covid-19 would be vast even if a large por­tion of the pop­u­la­tion is not sus­cep­ti­ble.
    ...

    And that points us to anoth­er kind of worst-case sce­nario we could be look­ing at: even if the efforts to com­bat the virus and it spreads around so much that we reach a “herd immu­ni­ty” lev­el of immu­ni­ty for the pop­u­la­tion, that herd immu­ni­ty does­n’t last because the virus is nev­er entire­ly stamped out and keeps mutat­ing and we still expe­ri­ence large-scale death in the most vul­ner­a­ble pop­u­la­tions each year.

    It’s also impor­tant to keep in mind that if this virus does end up becom­ing a per­ma­nent glob­al pan­dem­ic, there’s an alter­na­tive to soci­etal hyper-vig­i­lence: Just let the old and vul­ner­a­ble die off each year. Cre­ate a kind of A kind of “Logan’s Run” eugen­ics cul­ture, where it’s just accept­ed that if you are old and ‘weak’ you can and per­haps should be killed off by the virus. It’s an idea that’s gen­er­al­ly unthink­able for soci­ety at large these days but for the far right that’s like a dream sce­nario. So how long will it be before soci­eties just start col­lec­tive­ly say­ing “F#ck it! Let the weak die!” How many years of repeat­ed shut­down will it take before that becomes the atti­tu­di­nal norm? Hope­ful­ly we won’t have to ulti­mate­ly dis­cov­er that answer because a vac­cine will be devel­oped or herd immu­ni­ty will kick in. But if this real­ly is the ‘new nor­mal’ we’re look­ing at for the fore­see­able future we prob­a­bly should­n’t be sur­prised if that ‘new nor­mal’ includes a new moral par­a­digm for how we val­ue the lives of the sick and elder­ly. A new moral par­a­digm that isn’t all that new in some cir­cles.

    Posted by Pterrafractyl | May 15, 2020, 3:03 pm
  8. Now that the Trump admin­is­tra­tion announced “Oper­a­tion Warp Speed” — a crash pro­gram to devel­op a COVID-19 vac­cine — at the same time the pres­i­dent announces that Amer­i­ca is reopen­ing “vac­cine or no vac­cine”, here’s a New York Times Opin­ion piece from a month ago that gives a quick high-lev­el overview of dif­fer­ent long-term vac­cine sce­nar­ios that we can expect to play out.

    Unfor­tu­nate­ly, some of the warn­ings in the piece about the long-term chal­lenges fac­ing COVID vac­cines are now a lot more top­i­cal fol­low­ing that recent study out of Los Alam­os that found a dom­i­nant new “G” strain of SARS-CoV­‑2 that popped up in Europe (like­ly Ger­many) or Chi­na in late Jan­u­ary and rapid­ly came to become the dom­i­nant strain infect­ing Europe and the US, rapid­ly replac­ing the old­er “D” strain wher­ev­er they came in con­tact. Recall how the Los Alam­os researcher warned that their find­ings could have omi­nous impli­ca­tions for the devel­op­ment of a vac­cine. Why? Because the key muta­tion in the viral RNA they iden­ti­fied result­ed in an amino acid muta­tion in the virus’s spike-pro­tein, the cru­cial part of the virus where the active func­tion­al sites that facil­i­tate the infec­tion of cells is locat­ed.

    So why is a muta­tion in the spike pro­tein that appears to make the virus more infec­tious such an omi­nous find­ing? Well, as the fol­low­ing piece points out, if there’s going to be a sin­gle vac­cine that works in the long-run it’s going to have to tar­get the virus’s spike pro­tein so if the virus’s spike pro­tein has the abil­i­ty to mutate while still retain­ing its capac­i­ty to infect cells there won’t be a sin­gle vac­cine that can tack­le the virus. In some virus­es, like measles, the parts of the virus where the cru­cial inter­ac­tions with the cells take place are can’t sus­tain any muta­tions with­out los­ing their func­tion­al­i­ty. It’s an evo­lu­tion­ar­i­ly brit­tle virus in that sense. As a con­se­quence, the same measles vac­cine that was devel­oped in the 1950s still works today. Influen­za does­n’t have that vul­ner­a­bil­i­ty and can still func­tion with a vari­ety of muta­tions to its active sites. So if the dis­cov­ery of viable muta­tions in the spike pro­tein means the virus’s pro­tein-machin­ery has a vari­ety of viable options that sug­gests we’re look­ing at a per­ma­nent annu­al pan­dem­ic that nev­er goes away. It also sug­gests vac­cines might con­fer par­tial immu­ni­ty at best.

    Now, regard­ing the ongo­ing ques­tion of when and where this virus orig­i­nat­ed and the virus’s propen­si­ty to acquire func­tion­al muta­tions, it’s also worth recount­ing an inter­est­ing obser­va­tion from that ear­li­er study out of Cam­bridge where they found the Type A, B, and C strains, with Types B and C going on to dom­i­nate the infec­tions in Europe and then the US East Coast. Part of what pro­voked some back­lash to that study with­in the virol­o­gy com­mu­ni­ty was the sug­ges­tion by the researchers that their obser­va­tions that the Type B strains did­n’t mutat­ed very much as it spread across Asia com­pared to the muta­tion it was accru­ing in the Euro­pean pop­u­la­tion sug­gest­ed that the ini­tial muta­tions that defined the Type B strain had made the virus more adapt­ed to East Asian immune sys­tems but the virus had to con­tin­ue to adopt to Euro­pean immune sys­tems.
    So let’s assume those researchers were cor­rect and the ini­tial Type B strain reflect­ed some sort of adap­ta­tion in the virus that made it bet­ter suit­ed to com­bat Asian pop­u­la­tion immune sys­tems and con­tin­ued to acquire new muta­tions to help it deal with the immune sys­tem dif­fer­ences found in Europe. If that’s the case, we have to ask if the new “G” muta­tion found by the Los Alam­os team that seemed to pop up in Europe and Chi­na simul­ta­ne­ous­ly in late Jan­u­ary rep­re­sents one of those muta­tions that helped the Type B strain spread more eas­i­ly in Euro­pean pop­u­la­tions. The Cam­bridge team found the Type B strain dom­i­nat­ed the Euro­pean and US East Coast infec­tions and the Los Alam­os team found the “G” strain also came to dom­i­nate the Euro­pean and US East Cost infec­tions. So the “G” strain appears to be one of the branch­es of the ear­li­er “Type B” strain that appears to have popped up some time in Decem­ber.

    Here’s what poten­tial­ly quite inter­est­ing about that col­lec­tion of facts and infer­ences in rela­tion to the ques­tion of when and where this virus was first released: We appar­ent­ly saw the virus mutate an Asian-spe­cif­ic strain with­in about a month of two of the known out­break in Wuhan. Then that new strain jumps to Europe and a new Euro­pean-spe­cif­ic strain pops up a few weeks late. What does that time­frame tell us about how long this virus has been cir­cu­lat­ing among humans? One obvi­ous inter­pre­ta­tion is that the virus real­ly has only recent­ly start­ed cir­cu­lat­ing quite recent­ly and the rel­a­tive­ly rapid accu­mu­la­tion of what appear to be muta­tions that help deal with pop­u­la­tion-spe­cif­ic immune sys­tems is a reflec­tion of that recent expo­sure.

    If that’s the case and the virus real­ly has only recent­ly been exposed to humans — and this is all based on infer­ence and spec­u­la­tion at this point — it would have quite inter­est­ing impli­ca­tions respect to the grow­ing ques­tions about whether or not mil­i­tary ath­letes from France, Spain, and Italy were infect­ed with the coro­n­avirus at the Mil­i­tary World Games in Wuhan in late Octo­ber 2019. Because one of the big ques­tions raised from those reports of sick ath­letes is whether or not that meant the virus was cir­cu­lat­ing in Europe (or on mil­i­tary bases sta­tioned some­where) or else­where even ear­li­er last year. But if that was the case and it real­ly was Euro­pean ath­letes who brought the virus to Wuhan in Octo­ber, there’s the ques­tion of whether or not we should then expect the orig­i­nal strain in Wuhan to have already acquired those Euro­pean immune-spe­cif­ic muta­tions when it first showed up. In oth­er words, the orig­i­nal “Type A” strain should have already had the muta­tions the Cam­bridge team observed the Type B strain acquired as it pro­gressed through the Euro­pean pop­u­la­tions if we assume those Euro­pean mil­i­tary ath­letes picked up the virus from unde­tect­ed ear­li­er Euro­pean out­breaks. So if the mil­i­tary ath­letes were the source of this virus that would point toward them have been infect­ed with a very new strain that had just recent­ly start­ed spread­ing in humans. It’s a sce­nario that would be con­sis­tent with the idea of those ath­letes get­ting unwit­ting­ly used as vec­tors for an ini­tial viral release (some­thing that could have been pulled off from a wide vari­ety of actors).

    But again, we have to acknowl­edge that we have no idea at this point if these muta­tions real­ly are mak­ing the virus more infec­tious some­how or mak­ing it bet­ter at infect­ing spe­cif­ic pop­u­la­tions. That’s large­ly based on spec­u­la­tion and infer­ence at this point and it’s pos­si­ble the pat­tern of new strains over­tak­ing old ones is a con­se­quence of a “Founder effect” where ran­dom­ness is the dom­i­nant fac­tor. Although recall how the Los Alam­os study did actu­al­ly include a com­par­i­son of the viral loads in hos­pi­tal patients that had the “G” or “D” strains and found those with the new “G” strain had high­er viral loads. So it’s not entire­ly based on just spec­u­la­tion and infer­ence. There is some evi­dence that the new­er strain real­ly is some­how more infec­tious. But what is very clear at this point is that these muta­tions on the spike pro­tein are going to be cru­cial areas of study. If we’re lucky, and a sin­gle vac­cine is capa­ble of stop­ping this thing for good there’s going to be a flur­ry of study­ing of that spike pro­tein and then hope­ful­ly one day we can large­ly for­get it. But if we’re unlike­ly and this ends up being like the annu­al flu — but super-flu — there’s going to be a lot more focus on the spike pro­tein muta­tions for decades to come because the annu­al race for the vac­cine is going to depend on it:

    The New York Times
    Opin­ion

    The Coro­n­avirus Is Mutat­ing. What Does That Mean for a Vac­cine?

    By Nathaniel Lash and Tala Schloss­berg
    April 16, 2020

    Around the world, hope for a return to nor­mal­cy is pinned on a vac­cine, the “ulti­mate weapon,” as it’s been called by offi­cials like Dr. Antho­ny Fau­ci, direc­tor of the Nation­al Insti­tute of Aller­gy and Infec­tious Dis­eases. But it’s still unclear how suc­cess­ful a vac­cine against SARS-CoV­‑2, the virus that caus­es Covid-19, can be.

    A lot will depend on how the virus mutates. Broad­ly, there are two ways muta­tions can play out.

    Sce­nario 1: The coro­n­avirus is unable to evade a vac­cine

    A suc­cess­ful vac­cine could stop the virus dead in its tracks, but only if the virus does­n’t mutate its way around the shot. Here’s what sci­en­tists are watch­ing for:

    Like all virus­es, SARS-CoV­‑2 is mutat­ing as it pass­es from per­son to per­son. A “muta­tion” is just a change in a virus’s genet­ic code. Most muta­tions don’t real­ly change how the virus func­tions.

    Below is a glimpse at an imag­i­nary virus. It’s doing what all virus­es do: enter­ing a cell, hijack­ing the cell’s machin­ery and using it to make many copies of itself.

    ..

    Some­times, small errors — or muta­tions — can show up in that repli­ca­tion. Those errors accu­mu­late over time as the virus spreads from cell to cell and per­son to per­son.

    ...

    Vac­cines work by prompt­ing the body to devel­op anti­bod­ies, which neu­tral­ize the virus by bind­ing to it in a very spe­cif­ic way. Sci­en­tists are watch­ing to see if muta­tions will affect this inter­ac­tion. If they don’t, then there is hope that a vac­cine won’t need con­stant updat­ing.

    ...

    That same process has played out with our most effec­tive vac­cines, includ­ing the one against measles.

    Measles mutates just as fast as flu and coro­n­avirus, but the measles vac­cine from 1950 still works today,” said Trevor Bed­ford, a biol­o­gist at the Fred Hutchin­son Can­cer Research Cen­ter in Seat­tle.

    To enter a cell, the measles virus uses cer­tain of its pro­teins that are unable to mutate even slight­ly with­out break­ing. The vac­cine tar­gets those parts, so any muta­tion that would evade the vac­cine would mean that the virus can’t infect oth­er cells.

    The vac­cine has the measles virus cor­nered.

    Sce­nario 2: Muta­tions make vac­cines less effec­tive over time

    But what if the virus doesn’t get cor­nered like measles? If the virus mutates in a way that pre­vents anti­bod­ies from bind­ing, it could make a last­ing, uni­ver­sal vac­cine dif­fi­cult to cre­ate.

    Anti­bod­ies, which the body pro­duces in response to a vac­cine or an infec­tion, work by bind­ing to spe­cif­ic spots on a virus called anti­gens. If ran­dom viral muta­tions alter the shape of an anti­gen, it can make a vac­cine less effec­tive against the virus.

    “What will hap­pen in many virus­es is you’ll get infect­ed by Strain A; your immune sys­tem learns to rec­og­nize that sur­face pro­tein, but then the virus is able to mutate in such a fash­ion that it still per­forms its func­tion but make it so that your anti­bod­ies against Strain A no longer rec­og­nize Strain B,” Dr. Bed­ford said.

    Here’s that sce­nario play­ing out on our fic­tion­al virus: The anti­bod­ies pro­duced by the vac­cine work on one strain but can’t bind to the oth­er, ren­der­ing the vac­cine inef­fec­tive.

    That’s what hap­pens with the flu: The virus’s anti­gens mutate so much that they evolve into dif­fer­ent strains, each requir­ing a slight­ly dif­fer­ent vac­cine. Sci­en­tists con­tin­u­ous­ly devel­op vac­cines to tar­get those new strains. In spite of that, the vac­cines offer only par­tial immu­ni­ty to the var­i­ous flu strains that spread each year.

    If that hap­pens with the coro­n­avirus, researchers will have to rush to pro­duce and admin­is­ter new vac­cines as nov­el strains of the virus nat­u­ral­ly arise.

    It also reveals anoth­er quirk with how virus­es behave: Some can respond to the immu­ni­ty in the pop­u­la­tion they’re try­ing to infect. Over time, for exam­ple, many peo­ple devel­op immu­ni­ty to at least some strains of the flu — either through fight­ing off infec­tions or by get­ting vac­ci­nat­ed. But the virus keeps spread­ing. Here’s how.

    For a brand-new virus like SARS-CoV­‑2, there is no wide­spread immu­ni­ty. This virus is encoun­ter­ing few immune hosts who could halt its spread. Since the virus doesn’t need to change to sur­vive, muta­tions that could mod­i­fy the shape of the anti­gens — if they exist at all — are like­ly rare, and will stay rare.

    But if peo­ple become immune to the dom­i­nant strain, either by fight­ing off the virus or through vac­ci­na­tion, the game changes. Ver­sions of the virus with muta­tions that get around the population’s immu­ni­ty are more like­ly to spread, and can then devel­op into new strains.

    The take­away: We’ll have to wait and see

    Sci­en­tists know that SARS-CoV­‑2 is mutat­ing.

    Among the thou­sands of sam­ples of the long strand of RNA that makes up the coro­n­avirus, 11 muta­tions have become fair­ly com­mon. But as far as we know, it’s the same virus infect­ing peo­ple all over the world, mean­ing that only one “strain” of the virus exists, said Peter Thie­len, a mol­e­c­u­lar biol­o­gist with the Johns Hop­kins Applied Physics Lab­o­ra­to­ry.

    Only one of those com­mon muta­tions affects the “spike pro­tein,” which enables the virus to infect cells in the throat and lungs. Efforts to pro­duce anti­bod­ies that block the spike pro­tein are cen­tral to many efforts to devel­op a vac­cine. Since the spike pro­tein has changed lit­tle so far, some sci­en­tists believe that’s a sign that it can’t alter itself very much and remain infec­tious.

    There’s still a lot about the virus we don’t know. We don’t even know if peo­ple are immune to the virus if they’ve caught it already, nor how long that immu­ni­ty could last, though work is well under­way to under­stand these things.

    ...

    ———–

    “The Coro­n­avirus Is Mutat­ing. What Does That Mean for a Vac­cine?” by Nathaniel Lash and Tala Schloss­berg; The New York Times; 04/16/2020

    “Vac­cines work by prompt­ing the body to devel­op anti­bod­ies, which neu­tral­ize the virus by bind­ing to it in a very spe­cif­ic way. Sci­en­tists are watch­ing to see if muta­tions will affect this inter­ac­tion. If they don’t, then there is hope that a vac­cine won’t need con­stant updat­ing.”

    Watch­ing and wait­ing to see which muta­tions do what. That’s the hor­ri­ble wait­ing game we’re forced to play. A wait­ing game that will deter­mine whether or not this is a one-off pan­dem­ic or part of the ‘New Nor­mal’. And as they point out, if this ends up being an influen­za-type sce­nario where there’s a new vac­cine required each year, that vac­cine is only going to be con­fer­ring par­tial immu­ni­ty (and that’s assum­ing the vac­cine devel­op­ers do a good job guess­ing the upcom­ing strain). So it would be an annu­al vac­cine race that can only par­tial­ly be ‘won’ in the end any­way at best:

    ...
    Sce­nario 2: Muta­tions make vac­cines less effec­tive over time

    But what if the virus doesn’t get cor­nered like measles? If the virus mutates in a way that pre­vents anti­bod­ies from bind­ing, it could make a last­ing, uni­ver­sal vac­cine dif­fi­cult to cre­ate.

    Anti­bod­ies, which the body pro­duces in response to a vac­cine or an infec­tion, work by bind­ing to spe­cif­ic spots on a virus called anti­gens. If ran­dom viral muta­tions alter the shape of an anti­gen, it can make a vac­cine less effec­tive against the virus.

    ...

    Here’s that sce­nario play­ing out on our fic­tion­al virus: The anti­bod­ies pro­duced by the vac­cine work on one strain but can’t bind to the oth­er, ren­der­ing the vac­cine inef­fec­tive.

    That’s what hap­pens with the flu: The virus’s anti­gens mutate so much that they evolve into dif­fer­ent strains, each requir­ing a slight­ly dif­fer­ent vac­cine. Sci­en­tists con­tin­u­ous­ly devel­op vac­cines to tar­get those new strains. In spite of that, the vac­cines offer only par­tial immu­ni­ty to the var­i­ous flu strains that spread each year.

    If that hap­pens with the coro­n­avirus, researchers will have to rush to pro­duce and admin­is­ter new vac­cines as nov­el strains of the virus nat­u­ral­ly arise.
    ...

    And note the warn­ing that relates to hopes that “herd immu­ni­ty” will be achieved if we just allow the virus to spread rapid­ly across the pop­u­lace: The virus does­n’t real­ly have the same kind of selec­tive pres­sures on it right now that it will even­tu­al­ly have because the virus is new and human immune sys­tems weren’t ready for it. But that’s going to change if we ever hit a “herd immu­ni­ty” sta­tus, at which point virus’s abil­i­ty to spread will be chal­lenged enough that we would expect new strains to emerge by neces­si­ty if that’s an option for the virus. So while we should be con­cerned that these ear­ly muta­tions reflect the virus’s abil­i­ty to evolve to dif­fer­ent immune sys­tems, that’s a con­cern that should also grow the clos­er we get to herd immu­ni­ty if herd immu­ni­ty is the ulti­mate solu­tion to this:

    ...
    It also reveals anoth­er quirk with how virus­es behave: Some can respond to the immu­ni­ty in the pop­u­la­tion they’re try­ing to infect. Over time, for exam­ple, many peo­ple devel­op immu­ni­ty to at least some strains of the flu — either through fight­ing off infec­tions or by get­ting vac­ci­nat­ed. But the virus keeps spread­ing. Here’s how.

    For a brand-new virus like SARS-CoV­‑2, there is no wide­spread immu­ni­ty. This virus is encoun­ter­ing few immune hosts who could halt its spread. Since the virus doesn’t need to change to sur­vive, muta­tions that could mod­i­fy the shape of the anti­gens — if they exist at all — are like­ly rare, and will stay rare.

    But if peo­ple become immune to the dom­i­nant strain, either by fight­ing off the virus or through vac­ci­na­tion, the game changes. Ver­sions of the virus with muta­tions that get around the population’s immu­ni­ty are more like­ly to spread, and can then devel­op into new strains.
    ...

    Final­ly, note how it’s the spike pro­tein that’s going to be the tar­get of vac­cine devel­op­ment because that’s where the anti­bod­ies are going to tar­get. That’s why the Los Alam­os team issued their dire warn­ing about the new “G” strain seem­ing to have a greater lev­el of infec­tious­ness. The “G” muta­tion was on the spike pro­tein:

    ...
    Among the thou­sands of sam­ples of the long strand of RNA that makes up the coro­n­avirus, 11 muta­tions have become fair­ly com­mon. But as far as we know, it’s the same virus infect­ing peo­ple all over the world, mean­ing that only one “strain” of the virus exists, said Peter Thie­len, a mol­e­c­u­lar biol­o­gist with the Johns Hop­kins Applied Physics Lab­o­ra­to­ry.

    Only one of those com­mon muta­tions affects the “spike pro­tein,” which enables the virus to infect cells in the throat and lungs. Efforts to pro­duce anti­bod­ies that block the spike pro­tein are cen­tral to many efforts to devel­op a vac­cine. Since the spike pro­tein has changed lit­tle so far, some sci­en­tists believe that’s a sign that it can’t alter itself very much and remain infec­tious.
    ...

    Also note that the D‑to‑G muta­tion is the D614G which means it’s a muta­tion at the 614th amino acid in the spike pro­tein. That hap­pens to be loca­tion inside the spike pro­tein’s Recep­tor Bind­ing Domain (RBD). Specif­i­cal­ly between the Recep­tor Bind­ing Motif (RBM) that is cru­cial for bind­ing to the ACE2 recep­tor and the furin cleav­age site that acti­vates the virus. And that RBM area is going to be the key tar­get of the vac­cine-gen­er­at­ed anti­bod­ies so this muta­tion was pret­ty damn close to the vac­cine tar­get spot. That’s why it was such an omi­nous find­ing.

    As we can see, we already have an alarm­ing dis­cov­ery of a muta­tion that sug­gests this virus could be a key fea­ture of our ‘New Nor­mal’. A New Nor­mal that’s going to a new race for a new vac­cine year after year (assum­ing a par­tial­ly work­ing vac­cine is even pos­si­ble). Get ready for COVID-20, COVID-21, up to COVID-[we’ll see]! And this alarm­ing muta­tion might also be the sign that this virus has been strug­gling, suc­cess­ful­ly, to deal with dif­fer­ent Asian and Euro­pean immune sys­tems. A strug­gle that the virus seemed to over­come so rapid­ly that it sug­gests this virus real­ly did just get exposed to human pop­u­la­tions quite recent­ly because oth­er­wise it would have already acquired these muta­tions. And yet the real strug­gle has bare­ly begun for the virus because we haven’t yet reached herd immu­ni­ty. It’s still easy times for the virus. The hard part for the virus comes lat­er and that’s when we’re going to find out how vicious this thing can real­ly get. So we are already learn­ing that this virus appears to have options when it comes to infect­ing cells and the more options it has the more vicious it gets. The kind of viral options that could inher­ent­ly make both vac­ci­na­tion and herd immu­ni­ty a very lim­it­ed options for human­i­ty.

    That’s the bad news. But there’s still the good news: this virus is so demon­stra­bly good at infect­ing peo­ple it real­ly does­n’t have that much need to acquire more fea­tures than it already has. So this thing might be with us for a long time to come but at least it might not get much worse because it’s also ready so bad. It will just be con­sis­tent­ly awful for the fore­see­able future, which tech­ni­cal­ly could be worse.

    Posted by Pterrafractyl | May 16, 2020, 3:57 pm

Post a comment