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Modus Operandi of Covid-19–Does It Reflect Genetic Engineering?

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COMMENT: An inter­est­ing piece in “The Atlantic” describes how the SARS-CoV­‑2 virus that caus­es COVID-19 dif­fers from oth­er coro­n­avirus­es known to infect humans. We present this as sup­ple­men­tal to dis­cus­sion of DARPA research into bat-borne coro­n­avirus­es. Note that:

  1. The virus appears to have been a bat virus and the ran­dom muta­tions seen are unlike­ly to be nat­ur­al: ” . . . . What are the odds that a ran­dom bat virus had exact­ly the right com­bi­na­tion of traits to effec­tive­ly infect human cells from the get-go, and then jump into an unsus­pect­ing per­son? ‘Very low,’ [Kris­t­ian] Ander­sen [of the Scripps Research Trans­la­tion­al Insti­tute] says . . . . ”
  2. The SARS-CoV­‑2 (Covid-19) virus is unusu­al in that it infects both the upper and low­er res­pi­ra­to­ry tracts. The ‘spike’ part of the SARS-CoV­‑2 virus is unusu­al­ly good at latch­ing into a pro­tein called ACE2 which is found on the exte­ri­or of the cells in human air­ways. This abil­i­ty appears to be fun­da­men­tal to the virus’s abil­i­ty to infect the upper res­pi­ra­to­ry tract. The virus appears to infect the upper air­ways first and then, as cells in them die and are sloughed off, it makes its way down to the low­er res­pi­ra­to­ry tract and lungs where the dead­ly infec­tions occur. This sequen­tial pat­tern of infect­ing the upper res­pi­ra­to­ry tract pri­or to mak­ing its way down to the lungs enables it to silent­ly spread asymp­to­mati­cal­ly before turn­ing more lethal in the low­er res­pi­ra­to­ry tract.
  3. We note that the ACE2 pro­tein appears to man­i­fest more heav­i­ly in the lung tis­sue of  East-Asians. As indi­cat­ed in the Whit­ney Webb arti­cle, genet­ic mod­i­fi­ca­tion has been envi­sioned as applic­a­ble to bio­log­i­cal war­fare to cre­ate “eth­no-spe­cif­ic” bio­log­i­cal weapons.
  4. Anoth­er key fea­ture of the virus’s abil­i­ty to infect humans con­cerns a pro­tein bridge con­nect­ing two halves of the virus’s spike. Acti­va­tion of this spike caus­es the virus injects its nucle­ic acid into the cell. Acti­vat­ing the spike requires the cleav­age of a pro­tein bridge con­nect­ing the two halves of the spike. That cleav­age is pre­cip­i­tat­ed by the enzyme furin which is ubiq­ui­tous in human cells. In con­trast, the coro­n­avirus which caused SARS had a pro­tein bridge that was less like­ly to be cleaved. SARS-CoV­‑2 first latch­es onto to human upper air­way cells and, once there, has the pro­tein bridge link­ing the halves of the spike sev­ered by the furin enzyme.
  5. Per­haps the most notable obser­va­tion made about this virus thus far: it doesn’t appear to be mutat­ing in evo­lu­tion­ar­i­ly sig­nif­i­cant ways. Of the 100-plus muta­tions observed in the virus so far, none has emerged as evo­lu­tion­ar­i­ly dominant–unusual for a virus that only recent­ly jumped to humans. and has spread pro­lif­i­cal­ly. It’s as though the virus is already evo­lu­tion­ar­i­ly opti­mized for spread­ing among humans and there are no ‘gain-of-fuc­tion’ muta­tions left for it acquire. As Lisa Gralin­s­ki, a coro­n­avirus expert at the Uni­ver­si­ty of North Car­oli­na Chapel Hill, described it, “The virus has been remark­ably sta­ble giv­en how much trans­mis­sion we’ve seen . . . . there’s no evo­lu­tion­ary pres­sure on the virus to trans­mit bet­ter. It’s doing a great job of spread­ing around the world right now.”
  6.  Gralin­sky works close­ly with Ralph Baric’s lab. Recall that Bar­ic is the researcher who con­struct­ed a chimeric virus out of a SARS virus and horse­shoe bat coro­n­avirus in 2015. When Gralin­s­ki observes that the virus wouldn’t feel any evo­lu­tion­ary pres­sure to spread because it’s already doing such a good job that is VERY sig­nif­i­cant. Evo­lu­tion doesn’t stop just because the sta­tus quo of an organ­ism is already effec­tive. A muta­tion allow­ing the virus to spread even more read­i­ly would be expect­ed. And nor­mal­ly such an event does hap­pen. But it hasn’t hap­pened so for SARS-CoV­‑2 because it is already at some­thing of a “coro­n­avirus evo­lu­tion­ary peak”.

In addi­tion, an arti­cle in Sci­ence Direct char­ac­ter­izes the advent of the furin-like cleav­age site as a “gain-of-func­tion” phe­nom­e­non. “Gain of Func­tion” is a mech­a­nism of action of an “Enhanced Poten­tial Pan­dem­ic Pathogen.” “. . . . Strik­ing­ly, the 2019-nCoV S‑protein sequence con­tains 12 addi­tion­al nucleotides upstream of the sin­gle Arg↓ cleav­age site 1 (Fig. 1, Fig. 2) lead­ing to a pre­dic­tive­ly sol­vent-exposed PRRAR↓SV sequence, which cor­re­sponds to a canon­i­cal furin-like cleav­age site (Braun and Sauter, 2019; Iza­guirre, 2019; Sei­dah and Prat, 2012). This furin-like cleav­age site, is sup­posed to be cleaved dur­ing virus egress (Mille and Whit­tak­er, 2014) for S‑protein “prim­ing” and may pro­vide a gain-of-func­tion to the 2019-nCoV for effi­cient spread­ing in the human pop­u­la­tion com­pared to oth­er lin­eage b beta­coro­n­avirus­es. This pos­si­bly illus­trates a con­ver­gent evo­lu­tion path­way between unre­lat­ed CoVs. Inter­est­ing­ly, if this site is not processed, the S‑protein is expect­ed to be cleaved at site 2 dur­ing virus endo­cy­to­sis, as observed for the SARS-CoV. . . .”

1.  “Why the Coro­n­avirus Has Been So Suc­cess­ful” Ed Yong; The Atlantic; 03/20/2020

One of the few mer­cies dur­ing this cri­sis is that, by their nature, indi­vid­ual coro­n­avirus­es are eas­i­ly destroyed. Each virus par­ti­cle con­sists of a small set of genes, enclosed by a sphere of fat­ty lipid mol­e­cules, and because lipid shells are eas­i­ly torn apart by soap, 20 sec­onds of thor­ough hand-wash­ing can take one down. Lipid shells are also vul­ner­a­ble to the ele­ments; a recent study shows that the new coro­n­avirus, SARS-CoV­‑2, sur­vives for no more than a day on card­board, and about two to three days on steel and plas­tic. These virus­es don’t endure in the world. They need bod­ies.

But much about coro­n­avirus­es is still unclear. Susan Weiss, of the Uni­ver­si­ty of Penn­syl­va­nia, has been study­ing them for about 40 years. She says that in the ear­ly days, only a few dozen sci­en­tists shared her interest—and those num­bers swelled only slight­ly after the SARS epi­dem­ic of 2002. “Until then peo­ple looked at us as a back­ward field with not a lot of impor­tance to human health,” she says. But with the emer­gence of SARS-CoV‑2—the cause of the COVID-19 disease—no one is like­ly to repeat that mis­take again.

To be clear, SARS-CoV­‑2 is not the flu. It caus­es a dis­ease with dif­fer­ent symp­tomsspreads and kills more read­i­ly, and belongs to a com­plete­ly dif­fer­ent fam­i­ly of virus­es. This fam­i­ly, the coro­n­avirus­es, includes just six oth­er mem­bers that infect humans. Four of them—OC43, HKU1, NL63, and 229E—have been gen­tly annoy­ing humans for more than a cen­tu­ry, caus­ing a third of com­mon colds. The oth­er two—MERS and SARS (or “SARS-clas­sic,” as some virol­o­gists have start­ed call­ing it)—both cause far more severe dis­ease. Why was this sev­enth coro­n­avirus the one to go pan­dem­ic? Sud­den­ly, what we do know about coro­n­avirus­es becomes a mat­ter of inter­na­tion­al con­cern.

The struc­ture of the virus pro­vides some clues about its suc­cess. In shape, it’s essen­tial­ly a spiky ball. Those spikes rec­og­nize and stick to a pro­tein called ACE2, which is found on the sur­face of our cells: This is the first step to an infec­tion. The exact con­tours of SARS-CoV‑2’s spikes allow it to stick far more strong­ly to ACE2 than SARS-clas­sic did, and “it’s like­ly that this is real­ly cru­cial for per­son-to-per­son trans­mis­sion,” says Angela Ras­mussen of Colum­bia Uni­ver­si­ty. In gen­er­al terms, the tighter the bond, the less virus required to start an infec­tion.

There’s anoth­er impor­tant fea­ture. Coro­n­avirus spikes con­sist of two con­nect­ed halves, and the spike acti­vates when those halves are sep­a­rat­ed; only then can the virus enter a host cell. In SARS-clas­sic, this sep­a­ra­tion hap­pens with some dif­fi­cul­ty. But in SARS-CoV­‑2, the bridge that con­nects the two halves can be eas­i­ly cut by an enzyme called furin, which is made by human cells and—crucially—is found across many tis­sues. “This is prob­a­bly impor­tant for some of the real­ly unusu­al things we see in this virus,” says Kris­t­ian Ander­sen of Scripps Research Trans­la­tion­al Insti­tute.

For exam­ple, most res­pi­ra­to­ry virus­es tend to infect either the upper or low­er air­ways. In gen­er­al, an upper-res­pi­ra­to­ry infec­tion spreads more eas­i­ly, but tends to be milder, while a low­er-res­pi­ra­to­ry infec­tion is hard­er to trans­mit, but is more severe. SARS-CoV­‑2 seems to infect both upper and low­er air­ways, per­haps because it can exploit the ubiq­ui­tous furin. This dou­ble wham­my could also con­ceiv­ably explain why the virus can spread between peo­ple before symp­toms show up—a trait that has made it so dif­fi­cult to con­trol. Per­haps it trans­mits while still con­fined to the upper air­ways, before mak­ing its way deep­er and caus­ing severe symp­toms. All of this is plau­si­ble but total­ly hypo­thet­i­cal; the virus was only dis­cov­ered in Jan­u­ary, and most of its biol­o­gy is still a mys­tery.

The new virus cer­tain­ly seems to be effec­tive at infect­ing humans, despite its ani­mal ori­gins. The clos­est wild rel­a­tive of SARS-CoV­‑2 is found in bats, which sug­gests it orig­i­nat­ed in a bat, then jumped to humans either direct­ly or through anoth­er species. (Anoth­er coro­n­avirus found in wild pan­golins also resem­bles SARS-CoV­‑2, but only in the small part of the spike that rec­og­nizes ACE2; the two virus­es are oth­er­wise dis­sim­i­lar, and pan­golins are unlike­ly to be the orig­i­nal reser­voir of the new virus.) When SARS-clas­sic first made this leap, a brief peri­od of muta­tion was nec­es­sary for it to rec­og­nize ACE2 well. But SARS-CoV­‑2 could do that from day one. “It had already found its best way of being a [human] virus,” says Matthew Frie­man of the Uni­ver­si­ty of Mary­land School of Med­i­cine.

This uncan­ny fit will doubtless­ly encour­age con­spir­a­cy the­o­rists: What are the odds that a ran­dom bat virus had exact­ly the right com­bi­na­tion of traits to effec­tive­ly infect human cells from the get-go, and then jump into an unsus­pect­ing per­son? “Very low,” Ander­sen says, “but there are mil­lions or bil­lions of these virus­es out there. These virus­es are so preva­lent that things that are real­ly unlike­ly to hap­pen some­times do.”

Since the start of the pan­dem­ic, the virus hasn’t changed in any obvi­ous­ly impor­tant ways. It’s mutat­ing in the way that all virus­es do. But of the 100-plus muta­tions that have been doc­u­ment­ed, none has risen to dom­i­nance, which sug­gests that none is espe­cial­ly impor­tant. “The virus has been remark­ably sta­ble giv­en how much trans­mis­sion we’ve seen,” says Lisa Gralin­s­ki of the Uni­ver­si­ty of North Car­oli­na. “That makes sense, because there’s no evo­lu­tion­ary pres­sure on the virus to trans­mit bet­ter. It’s doing a great job of spread­ing around the world right now.”

There’s one pos­si­ble excep­tion. A few SARS-CoV­‑2 virus­es that were iso­lat­ed from Sin­ga­pore­an COVID-19 patients are miss­ing a stretch of genes that also dis­ap­peared from SARS-clas­sic dur­ing the late stages of its epi­dem­ic. This change was thought to make the orig­i­nal virus less vir­u­lent, but it’s far too ear­ly to know whether the same applies to the new one. Indeed, why some coro­n­avirus­es are dead­ly and some are not is unclear. “There’s real­ly no under­stand­ing at all of why SARS or SARS-CoV­‑2 are so bad but OC43 just gives you a run­ny nose,” Frie­man says.

Researchers can, how­ev­er, offer a pre­lim­i­nary account of what the new coro­n­avirus does to the peo­ple it infects. Once in the body, it like­ly attacks the ACE2-bear­ing cells that line our air­ways. Dying cells slough away, fill­ing the air­ways with junk and car­ry­ing the virus deep­er into the body, down toward the lungs. As the infec­tion pro­gress­es, the lungs clog with dead cells and flu­id, mak­ing breath­ing more dif­fi­cult. (The virus might also be able to infect ACE2-bear­ing cells in oth­er organs, includ­ing the gut and blood ves­sels.)

The immune sys­tem fights back and attacks the virus; this is what caus­es inflam­ma­tion and fever. But in extreme cas­es, the immune sys­tem goes berserk, caus­ing more dam­age than the actu­al virus. For exam­ple, blood ves­sels might open up to allow defen­sive cells to reach the site of an infec­tion; that’s great, but if the ves­sels become too leaky, the lungs fill even more with flu­id. These dam­ag­ing over­re­ac­tions are called cytokine storms. They were his­tor­i­cal­ly respon­si­ble for many deaths dur­ing the 1918 flu pan­dem­ic, H5N1 bird flu out­breaks, and the 2003 SARS out­break. And they’re prob­a­bly behind the most severe cas­es of COVID-19. “These virus­es need time to adapt to a human host,” says Akiko Iwasa­ki of the Yale School of Med­i­cine. “When they’re first try­ing us out, they don’t know what they’re doing, and they tend to elic­it these respons­es.”

Dur­ing a cytokine storm, the immune sys­tem isn’t just going berserk but is also gen­er­al­ly off its game, attack­ing at will with­out hit­ting the right tar­gets. When this hap­pens, peo­ple become more sus­cep­ti­ble to infec­tious bac­te­ria. The storms can also affect oth­er organs besides the lungs, espe­cial­ly if peo­ple already have chron­ic dis­eases. This might explain why some COVID-19 patients end up with com­pli­ca­tions such as heart prob­lems and sec­ondary infec­tions.

But why do some peo­ple with COVID-19 get incred­i­bly sick, while oth­ers escape with mild or nonex­is­tent symp­toms? Age is a fac­tor. Elder­ly peo­ple are at risk of more severe infec­tions pos­si­bly because their immune sys­tem can’t mount an effec­tive ini­tial defense, while chil­dren are less affect­ed because their immune sys­tem is less like­ly to progress to a cytokine storm. But oth­er factors—a person’s genes, the vagaries of their immune sys­tem, the amount of virus they’re exposed to, the oth­er microbes in their bodies—might play a role too. In gen­er­al, “it’s a mys­tery why some peo­ple have mild dis­ease, even with­in the same age group,” Iwasa­ki says.

Coro­n­avirus­es, much like influen­za, tend to be win­ter virus­es. In cold and dry air, the thin lay­ers of liq­uid that coat our lungs and air­ways become even thin­ner, and the beat­ing hairs that rest in those lay­ers strug­gle to evict virus­es and oth­er for­eign par­ti­cles. Dry air also seems to damp­en some aspects of the immune response to those trapped virus­es. In the heat and humid­i­ty of sum­mer, both trends reverse, and res­pi­ra­to­ry virus­es strug­gle to get a foothold.

Unfor­tu­nate­ly, that might not mat­ter for the COVID-19 pan­dem­ic. At the moment, the virus is tear­ing through a world of immuno­log­i­cal­ly naive peo­ple, and that vul­ner­a­bil­i­ty is like­ly to swamp any sea­son­al vari­a­tions. After all, the new virus is trans­mit­ting read­i­ly in coun­tries like Sin­ga­pore (which is in the trop­ics) and Aus­tralia (which is still in sum­mer). And one recent mod­el­ing study con­clud­ed that “SARS-CoV­‑2 can pro­lif­er­ate at any time of year.” “I don’t have an immense amount of con­fi­dence that the weath­er is going to have the effect that peo­ple hope it will,” Gralin­s­ki says. “It may knock things down a lit­tle, but there’s so much per­son-to-per­son trans­mis­sion going on that it may take more than that.” Unless peo­ple can slow the spread of the virus by stick­ing to phys­i­cal-dis­tanc­ing rec­om­men­da­tions, the sum­mer alone won’t save us.

2. “The Spike Gly­co­pro­tein of the New Coro­n­avirus 2019-nCov Con­tains a Furin-Like Cleav­age Site Absent in CoV of the Same Clade” by B. Coutard, C. Valle, B. Canard, N.G. Sei­dah, E. Decroly et al.; Sci­ence Direct; Vol. 176: April 2020.

. . . . Based on its genome sequence, 2019-nCoV belongs to lin­eage b of Beta­coro­n­avirus (Fig. 1A), which also includes the SARS-CoV and bat CoV ZXC21, the lat­ter and CoV ZC45 being the clos­est to 2019-nCoV.  . . .

. . . . Since furin is high­ly expressed in lungs, an enveloped virus that infects the res­pi­ra­to­ry tract may suc­cess­ful­ly exploit this con­ver­tase to acti­vate its sur­face gly­co­pro­tein (Bassi et al., 2017Mbikay et al., 1997). Before the emer­gence of the 2019-nCoV, this impor­tant fea­ture was not observed in the lin­eage b of beta­coro­n­avirus­es. How­ev­er, it is shared by oth­er CoV (HCoV-OC43, MERS-CoV, MHV-A59) har­bour­ing furin-like cleav­age sites in their S‑protein (Fig. 2Table 1), which were shown to be processed by furin exper­i­men­tal­ly (Le Coupanec et al., 2015Mille and Whit­tak­er, 2014.

Strik­ing­ly, the 2019-nCoV S‑protein sequence con­tains 12 addi­tion­al nucleotides upstream of the sin­gle Arg↓ cleav­age site 1 (Fig. 1, Fig. 2) lead­ing to a pre­dic­tive­ly sol­vent-exposed PRRAR↓SV sequence, which cor­re­sponds to a canon­i­cal furin-like cleav­age site (Braun and Sauter, 2019; Iza­guirre, 2019; Sei­dah and Prat, 2012). This furin-like cleav­age site, is sup­posed to be cleaved dur­ing virus egress (Mille and Whit­tak­er, 2014) for S‑protein “prim­ing” and may pro­vide a gain-of-func­tion to the 2019-nCoV for effi­cient spread­ing in the human pop­u­la­tion com­pared to oth­er lin­eage b beta­coro­n­avirus­es. This pos­si­bly illus­trates a con­ver­gent evo­lu­tion path­way between unre­lat­ed CoVs. Inter­est­ing­ly, if this site is not processed, the S‑protein is expect­ed to be cleaved at site 2 dur­ing virus endo­cy­to­sis, as observed for the SARS-CoV. . . .

Discussion

13 comments for “Modus Operandi of Covid-19–Does It Reflect Genetic Engineering?”

  1. Sure you’ve already seen these but on the off chance that you’ve not:

    Tiergartenstrasse4 for the 21st cen­tu­ry?:

    https://www.usatoday.com/story/news/nation/2020/03/26/coronavirus-crisis-people-with-disabilities-discriminate/5082197002/

    https://www.nytimes.com/2020/03/24/upshot/coronavirus-rationing-decisions-ethicists.html

    “Cap­i­tal­ist colony col­lapse”:

    https://www.cnbc.com/2020/03/18/bill-ackman-pleads-to-trump-to-increase-closures-to-save-the-economy-shut-it-down-now.html

    Investor Bill Ack­man urged Pres­i­dent Don­ald Trump and cor­po­rate Amer­i­ca in an impas­sioned plea on CNBC to shut down the coun­try for 30 days to con­tain the fast-spread­ing coro­n­avirus, call­ing it the only option to res­cue the econ­o­my.

    “What’s scar­ing the Amer­i­can peo­ple and cor­po­rate Amer­i­ca now is the grad­ual roll­out,” Ack­man told Scott Wap­n­er on “Half­time Report” on Wednes­day. “We need to shut it down now. ... This is the only answer.”

    Amer­i­ca will end as we know it. I’m sor­ry to say so, unless we take this option,” he said. Ack­man added that if Trump saves the coun­try from the coro­n­avirus, he will get reelect­ed in Novem­ber.

    Ack­man urged U.S. com­pa­nies to stop their buy­back pro­grams because “hell is com­ing.” The biggest U.S. banks have already halt­ed repur­chas­ing stocks to put their cap­i­tal to use help­ing con­sumers and busi­ness­es.

    Black swans and black eagles?

    https://www.forbes.com/sites/kenrapoza/2020/01/10/dont-discount-a-black-swan-event-for-china/

    https://www.cnn.com/2019/12/15/investing/stocks-week-ahead/index.html

    Posted by Peter Pandemic | March 27, 2020, 9:10 am
  2. @Peter Pan­dem­ic: There’s an inter­est­ing fol­low­ing con­tro­ver­sy relat­ed to Bill Ack­man’s CNBC appear­ance where he warned that “Amer­i­ca will end as we know it” unless Pres­i­dent Trump shuts the US econ­o­my down for 30 days to get the spread of COVID-19 under con­trol: The mar­kets start­ed tank­ing even more aggres­sive­ly dur­ing Ack­man’s apoc­a­lyp­tic inter­view. CNBC’s Stephanie Fuuh­le lat­er chas­tised Ack­man for being wild­ly irre­spon­si­ble with his com­ments and caus­ing the cir­cuit-break­ers to trig­ger. This prompt­ed a num­ber of observers to point out that Ack­man’s firm, Per­sh­ing Square Cap­i­tal, hap­pened to have dis­closed on March 3 that it had opened up a num­ber of aggres­sive short posi­tions in the mar­ket that were designed to prof­it from a desta­bi­liza­tion of the cred­it mar­kets. This led to accu­sa­tions that Ack­man deci­sion to call into CNBC and make his apoc­a­lyp­tic com­ments was intend­ed to fur­ther desta­bi­lize the mar­kets and prof­it from those short posi­tions.

    Ack­man defends him­self against these accu­sa­tions by sug­gest­ing that he had actu­al­ly become bull­ish due to his belief that a US lock­down was com­ing soon and that this defeat the virus. It’s not exact­ly a com­pelling defense.

    Ack­man also point­ed out that Per­sh­ing Square Cap­i­tal had actu­al­ly already start­ed buy­ing up stocks in areas like hotel and trav­el stocks as the mar­ket was declin­ing. Dur­ing that inter­view he warned that hotel stocks would go to zero if the 30 day lock­down did­n’t hap­pen soon. by point­ing out that he was already start­ing to buy up the hotel stocks that had already been ham­mered, Ack­man appeared to be argu­ing that he would­n’t have had an incen­tive to dri­ve down the mar­ket since his hedge fund was already long on the very types of stocks he was warn­ing would “go to zero” dur­ing the CNBC call. It’s not exact­ly a com­pelling defense since going long on those stocks implies that the hedge fund thinks they’ll be going even high­er in the future so there’s actu­al­ly an incen­tive to tem­porar­i­ly dri­ve the stocks even low­er so you can buy them even cheap­er. For exam­ple, let’s say the val­ue of HotelX chain had fall­en from $100/share to $80/share duing a peri­od when Per­sh­ing Square Cap­i­tal was buy­ing the stock. That would sug­gest the fund expects HotelX’s stock to be above $100 at some point in the future. And if that’s the case, Per­sh­ing Square Cap­i­tal would have had an incen­tive to dri­ve HotelX’s stock down as low as pos­si­ble to buy up more shares for even cheap­er. Dri­ving HotelX’s stock down to $50/share would only make it even more tempt­ing a buy if you think it’s going to go back above $100, espe­cial­ly if you’re already short­ing the mar­kets and pro­tect­ing against those loss­es.

    But the big sto­ry here does­n’t real­ly have to do with Per­sh­ing Square Cap­i­tal. The big sto­ry is about just how wild­ly prof­itable those short posi­tions were as an exam­ple of how much mon­ey some­one could have if they made big bets on a large desta­bi­liza­tion of the econ­o­my before it was clear this virus was going to shut down the glob­al econ­o­my: Ack­man’s firm made $2.6 bil­lion on short posi­tions that it spent $27 mil­lion on. That’s a ~100-fold return.

    It sounds like, net, Per­sh­ing Square Cap­i­tal’s short posi­tions basi­cal­ly cov­ered the loss­es it’s made on its long posi­tions. At least for the time being. If the mar­ket recov­ers there’s pre­sum­ably going to be quite a prof­it on those stocks the fund has been buy­ing on the way down. But you have to won­der how many oth­er firms out that did­n’t sim­ply cov­er their loss­es but actu­al­ly made large net returns short­ing the mar­kets in a sim­i­lar fash­ion

    Ok, first, here’s an arti­cle where Ack­man attempts to defend him­self against accu­sa­tions that he was inten­tion­al­ly dri­ving down the mar­ket. Ack­man asserts that, con­trary to what every­one is say­ing, he was actu­al­ly being bull­ish in his com­ments. Plus, since his fund was buy­ing up stocks on the way down that means the accu­sa­tions he was try­ing to dri­ve down the mar­ket was absurd. So his warn­ings about hotel stocks “going to zero” were actu­al­ly bull­ish because he was buy­ing upon those very same plum­met­ing stocks he was warn­ing would go to zero Which is a pret­ty absurd defense but that’s what he’s argu­ing:

    CNBC

    Bill Ack­man says accu­sa­tions he tried to dri­ve down mar­ket in inter­view are ‘absurd’

    Thomas Franck
    Pub­lished Fri, Mar 27 2020 10:03 AM EDT
    Updat­ed Fri, Mar 27 202012:42 PM EDT

    * “The idea that my appear­ance pushed the mar­ket down an addi­tion­al 4% that day is absurd,” Ack­man told investors on Thurs­day.
    * Ack­man urged the White House on March 18 to seal off the U.S. to pro­tect the Amer­i­can pop­u­la­tion from the coro­n­avirus before his inter­view on CNBC.
    * The impas­sioned and warn­ing-full inter­view sparked con­tro­ver­sy as oth­er investors argued that his fund would prof­it from fur­ther mar­ket declines.

    Per­sh­ing Square Cap­i­tal man­ag­er Bill Ack­man defend­ed his emo­tion­al CNBC appear­ance last week after his fund announced a few days lat­er that it made more than $2 bil­lion on bets against the mar­kets. The investor warned in the inter­view that “hell is com­ing” and that hotel stocks could go to zero.

    “Short­ly after the show, I heard that some had inter­pret­ed my remarks as being very bear­ish on the mar­ket,” Ack­man told investors on Thurs­day. “The idea that my appear­ance pushed the mar­ket down an addi­tion­al 4% that day is absurd.”

    “Yes, I got some­what emo­tion­al as I talked about pro­tect­ing my immune-com­pro­mised father from the rav­ages of the virus. But, I had become bull­ish because of my belief that the entire coun­try would soon go into lock­down, and that would be the fastest and best way to min­i­mize the impact of the virus,” he added.

    The bil­lion­aire investor had urged Pres­i­dent Don­ald Trump on March 18 on Twit­ter to seal off the U.S. from the rest of the world “for the next 30 days” to pro­tect the Amer­i­can pop­u­la­tion from fur­ther coro­n­avirus destruc­tion before join­ing CNBC’s Scott Wap­n­er lat­er that day.

    With expo­nen­tial com­pound­ing, every day we post­pone the shut­down costs thou­sands, and soon hun­dreds of thou­sands, and then mil­lions of lives, and destroys the econ­o­my.— Bill Ack­man (@BillAckman) March 18, 2020

    At that time, Ack­man warned that hotel oper­a­tor Hilton World­wide was “going to zero ... along with every oth­er hotel com­pa­ny in the world,” said that Amer­i­ca could “end as we know it” and cau­tioned U.S. com­pa­nies to stop their stock buy­back pro­grams because “hell is com­ing.”

    The impas­sioned inter­view sparked con­tro­ver­sy, how­ev­er, as oth­er investors argued that Per­sh­ing would prof­it from fur­ther mar­ket declines thanks to a series of pre­scient bets made in Feb­ru­ary. Ack­man dis­closed on March 3 that he’d pur­chased a vari­ety of cred­it default swaps on invest­ment-grade and high-yield index­es, essen­tial­ly pur­chas­ing insur­ance on cred­it which would increase in val­ue as the under­ly­ing assets dete­ri­o­rat­ed and spreads widened.

    Ack­man explained on March 3 that he’d pur­chased the default swaps as hedges against the mar­ket if efforts to con­tain the nov­el coro­n­avirus had a “sub­stan­tial neg­a­tive impact on the U.S. and glob­al economies” as he thought like­ly. But some argued that his appear­ance March 18 on CNBC was intend­ed to sow fur­ther fear and increase the val­ue of the swaps.

    “A num­ber of press reports have raised ques­tions about my appear­ance on CNBC last Wednes­day, and some have even ques­tioned whether my appear­ance was intend­ed to dri­ve down the mar­ket so that we could prof­it on hedges we had pre­vi­ous­ly entered into,” Ack­man wrote in the let­ter.

    But Ack­man reit­er­at­ed that he had said in the inter­view on March 18 that he had already start­ed adding to Pershing’s exist­ing stock hold­ings since equi­ties looked cheap amid the his­toric mar­ket sell-off.

    That is why we are buy­ing stocks. These are bar­gains of a life­time if we man­age this cri­sis cor­rect­ly.— Bill Ack­man (@BillAckman) March 18, 2020

    That is why we are buy­ing stocks. These are bar­gains of a life­time if we man­age this cri­sis cor­rect­ly.— Bill Ack­man (@BillAckman) March 18, 2020

    That is why we are buy­ing stocks. These are bar­gains of a life­time if we man­age this cri­sis cor­rect­ly.— Bill Ack­man (@BillAckman) March 18, 2020

    “My bull­ish pos­ture and my state­ments on CNBC and Twit­ter were strong­ly sup­port­ive of the mar­kets. I made those state­ments at the time we were buy­ing stocks and reduc­ing our short in the cred­it mar­kets,” Ack­man wrote Thurs­day.

    Ack­man said in his let­ter that his hedge had already paid off pri­or to his appear­ance on CNBC and that Per­sh­ing had sold most, but not all, of the hedge pri­or to his inter­view with Wap­n­er.

    ...

    ————

    “Bill Ack­man says accu­sa­tions he tried to dri­ve down mar­ket in inter­view are ‘absurd’” by Thomas Franck; CNBC; 03/27/2020

    “Per­sh­ing Square Cap­i­tal man­ag­er Bill Ack­man defend­ed his emo­tion­al CNBC appear­ance last week after his fund announced a few days lat­er that it made more than $2 bil­lion on bets against the mar­kets. The investor warned in the inter­view that “hell is com­ing” and that hotel stocks could go to zero.

    “Hell is com­ing” and hotel stocks could go to zero, unless Trump impos­es a 30 day lock­down. That was mes­sage 10 days ago dur­ing the CNBC inter­view. But the way Ack­man describes it, he was actu­al­ly bull­ish at the time and had start­ed buy­ing up cheap hotel stocks because he was con­fi­dent the entire US would soon go into lock­down soon. And then he also notes that his fund had already unwound most, but not all, of its short posi­tions by the time of the inter­view. It’s not exact­ly a com­pelling defense:

    ...
    “Short­ly after the show, I heard that some had inter­pret­ed my remarks as being very bear­ish on the mar­ket,” Ack­man told investors on Thurs­day. “The idea that my appear­ance pushed the mar­ket down an addi­tion­al 4% that day is absurd.”

    “Yes, I got some­what emo­tion­al as I talked about pro­tect­ing my immune-com­pro­mised father from the rav­ages of the virus. But, I had become bull­ish because of my belief that the entire coun­try would soon go into lock­down, and that would be the fastest and best way to min­i­mize the impact of the virus,” he added.

    ...

    “A num­ber of press reports have raised ques­tions about my appear­ance on CNBC last Wednes­day, and some have even ques­tioned whether my appear­ance was intend­ed to dri­ve down the mar­ket so that we could prof­it on hedges we had pre­vi­ous­ly entered into,” Ack­man wrote in the let­ter.

    But Ack­man reit­er­at­ed that he had said in the inter­view on March 18 that he had already start­ed adding to Pershing’s exist­ing stock hold­ings since equi­ties looked cheap amid the his­toric mar­ket sell-off.

    ...

    “My bull­ish pos­ture and my state­ments on CNBC and Twit­ter were strong­ly sup­port­ive of the mar­kets. I made those state­ments at the time we were buy­ing stocks and reduc­ing our short in the cred­it mar­kets,” Ack­man wrote Thurs­day.

    Ack­man said in his let­ter that his hedge had already paid off pri­or to his appear­ance on CNBC and that Per­sh­ing had sold most, but not all, of the hedge pri­or to his inter­view with Wap­n­er.
    ...

    And now here’s an arti­cle that points out just how wild­ly prof­itable those short posi­tions real­ly were: $2.6 bil­lion on $27 mil­lion. That’s how pre­scient the bet was that Per­sh­ing Square Cap­i­tal made back in Feb­ru­ary. The spe­cif­ic bet was far ‘out of the mon­ey’ pro­tec­tion against invest­ment-grade and high-yield bond index­es. So, basi­cal­ly, that $27 mil­lion was unlike­ly to make any mon­ey at all unless there was a large dis­rup­tion in the cor­po­rate cred­it mar­kets at which point they could be worth quite a bit. It was a high-pay­out/low-prob­a­bilty bet which means those shorts were going to be extra cheap. Implic­it­ly, it also means the rest of the mar­ket was not bet­ting on the lev­el of finan­cial upheaval that unfold­ed. That’s why the options were so cheap and what allowed for the 100-fold pay­out and why it’s now deemed to be a high­ly pre­scient bet.

    In the case of Per­sh­ing Square Cap­i­tal this bet is seen as being even more pre­scient than it would be for oth­er hedge funds because Per­sh­ing Square almost exclu­sive­ly makes long bets on a hand­ful of hold­ings. That’s the fund’s gen­er­al strat­e­gy: find sev­en or eight com­pa­nies that Ack­man has faith in and make $500-to-$1 bil­lion invest­ments in those com­pa­nies. The fund isn’t known for tak­ing short posi­tions. But So you have to won­der just who else made sim­i­lar out of the mon­ey bets wih 100-fold returns over the past month

    Forbes

    Bil­lion­aire Bill Ack­man Made 100-Fold Return On Coro­n­avirus Hedge That Yield­ed $2.6 Bil­lion

    Antoine Gara Forbes Staff
    Mar 25, 2020, 08:42am EDT

    Bill Ack­man is a hedge fund bil­lion­aire, but he isn’t known for his hedges.

    Most of the time Ackman’s fund, Per­sh­ing Square, is almost 100% long by way of an ultra-con­cen­trat­ed port­fo­lio of large stock hold­ings. His cur­rent style is to find about sev­en-or-eight com­pa­nies he believes strong­ly in and bet between $500 mil­lion and $1 bil­lion on each.

    So when Ack­man decid­ed to pro­tect Per­sh­ing Square’s $6.5 bil­lion port­fo­lio of stock hold­ings in com­pa­nies from Chipo­tle to Berk­shire Hath­away and Lowe’s, it was out of the ordi­nary. By the end of Feb­ru­ary, Ack­man had come to believe that the coro­n­avirus pan­dem­ic was a mas­sive risk for the Unit­ed States, its econ­o­my, and glob­al finan­cial mar­kets.

    He and his traders spent $27 mil­lion buy­ing all the port­fo­lio pro­tec­tion they could find. Ulti­mate­ly, they focused on cred­it mar­kets. With spreads that are a gauge of risk­i­ness and fear at record lows, Per­sh­ing Square bought far out of the mon­ey pro­tec­tion against invest­ment-grade and high-yield bond index­es. The hedges were designed to pro­tect Per­sh­ing Square against an explo­sion of risk and volatil­i­ty if the coro­n­avirus spread. If that hap­pened, they expect­ed spreads to widen enor­mous­ly, putting their ultra-con­vex bets into-the-mon­ey and pro­tect­ing their port­fo­lio against a sharp draw­down in equi­ty mar­kets.

    The hedges worked bril­liant­ly. The S&P 500 Index has shed about a quar­ter of its val­ue in a month, but Ack­man did fine.

    As of Wednesday’s close, Per­sh­ing Square was up 0.2% for the year, ver­sus the 2o%-plus plunge of the S&P 500. His hedges shield­ed his investors against 50%-plus declines in some of his hold­ings. The maneu­ver­ing has pro­tect­ed all of the 58% gain Per­sh­ing Square report­ed to its investors in 2019.

    On Mon­day, after a some­what ques­tion­able deci­sion to call into CNBC and out­line just how bad the virus could be for the econ­o­my and how hard com­pa­nies might get hit, Ack­man took off the hedges.

    He’d judged that gov­er­nors across Amer­i­ca and offi­cials in Wash­ing­ton were tak­ing the right steps to com­bat the spread of the pan­dem­ic and sup­port the U.S. econ­o­my. The wind­fall was enor­mous. The $27 mil­lion he spent on pro­tec­tion had turned into $2.6 bil­lion.

    Ack­man isn’t one to move slow­ly. In about a day, he then spent about $1.5 bil­lion re-build­ing a posi­tion in Star­bucks, and adding to com­pa­nies like Agi­lent, Berk­shire Hath­away, Hilton, Lowe’s and Restau­rant Brands, the par­ent com­pa­ny of Burg­er King and Popeye’s. He con­tin­ues to sit on about $1 bil­lion in cash that still can be deployed as con­tain­ment, or even recov­ery, becomes more evi­dent.

    “We con­tin­ue to expect that mar­kets (and our per­for­mance) will remain volatile, and there­fore, new oppor­tu­ni­ties may present them­selves that are supe­ri­or to invest­ments we cur­rent­ly own,” Ack­man told his investors in a Tues­day morn­ing let­ter. “This may lead us to sell cer­tain of our exist­ing hold­ings includ­ing invest­ments we recent­ly pur­chased. We may also choose to reestab­lish sim­i­lar or dif­fer­ent forms of hedges or raise more cash based on devel­op­ments with the coro­n­avirus and oth­er mar­ket fac­tors. In oth­er words, we are more like­ly to have high­er port­fo­lio turnover in this envi­ron­ment.”

    Ack­man dis­closed that his $400 mil­lion Per­sh­ing Square Foun­da­tion, known for its impact invest­ing phi­los­o­phy, has invest­ed cap­i­tal in a com­pa­ny called Cov­axx, which is work­ing to boost anti­body test­ing kits to test peo­ple against the coro­n­avirus dis­ease.

    “We are in one of the most chal­leng­ing peri­ods of time for our coun­try, and for the world. Thou­sands of peo­ple have or will soon become severe­ly sick, and many will die,” added Ack­man about the pan­dem­ic, “This is a tragedy that could have been pre­vent­ed with bet­ter long-term plan­ning, which should have begun more than a decade ago. I have always said that expe­ri­ence is mak­ing mis­takes and learn­ing from them. And learn from this we must.”

    ...

    ————

    “Bil­lion­aire Bill Ack­man Made 100-Fold Return On Coro­n­avirus Hedge That Yield­ed $2.6 Bil­lion” by Antoine Gara; Forbes; 03/25/2020

    Most of the time Ackman’s fund, Per­sh­ing Square, is almost 100% long by way of an ultra-con­cen­trat­ed port­fo­lio of large stock hold­ings. His cur­rent style is to find about sev­en-or-eight com­pa­nies he believes strong­ly in and bet between $500 mil­lion and $1 bil­lion on each.”

    Ack­man’s hedge fund is almost 100% long in ultra-con­cen­trat­ed posi­tions in just sev­en or eight com­pa­nies. That’s part of what made this short posi­tion unusu­al. But it was a posi­tion that was still just a tiny frac­tion of the fund’s $6.5 bil­lion port­fo­lio: only $27 mil­lion was spent on these far “out of the mon­ey” short posi­tions that increased in val­ue if the spread between low risk and high risk lend­ing jumped. It was basi­cal­ly an eco­nom­ic dooms­day bet that paid off:

    ...
    So when Ack­man decid­ed to pro­tect Per­sh­ing Square’s $6.5 bil­lion port­fo­lio of stock hold­ings in com­pa­nies from Chipo­tle to Berk­shire Hath­away and Lowe’s, it was out of the ordi­nary. By the end of Feb­ru­ary, Ack­man had come to believe that the coro­n­avirus pan­dem­ic was a mas­sive risk for the Unit­ed States, its econ­o­my, and glob­al finan­cial mar­kets.

    He and his traders spent $27 mil­lion buy­ing all the port­fo­lio pro­tec­tion they could find. Ulti­mate­ly, they focused on cred­it mar­kets. With spreads that are a gauge of risk­i­ness and fear at record lows, Per­sh­ing Square bought far out of the mon­ey pro­tec­tion against invest­ment-grade and high-yield bond index­es. The hedges were designed to pro­tect Per­sh­ing Square against an explo­sion of risk and volatil­i­ty if the coro­n­avirus spread. If that hap­pened, they expect­ed spreads to widen enor­mous­ly, putting their ultra-con­vex bets into-the-mon­ey and pro­tect­ing their port­fo­lio against a sharp draw­down in equi­ty mar­kets.

    The hedges worked bril­liant­ly. The S&P 500 Index has shed about a quar­ter of its val­ue in a month, but Ack­man did fine.
    ...

    And note it also sounds like Per­sh­ing invest­ed in a new coro­n­avirus anti­body test kit com­pa­ny, Cov­axx. Keep in mind that wide­spread anti­body tests are actu­al­ly extreme­ly impor­tant for deal­ing with the cur­rent pan­dem­ic and allow­ing economies to nor­mal­ize. It’s those kinds of tests that will allow us to know who has been exposed to the virus and hope­ful­ly has immu­ni­ty. So if Cov­axx does end up devel­op­ing a work­able test that becomes part of the solution...well, at least in that case it will be a decent way to prof­it from this eco­nom­ic night­mare:

    ...
    Ack­man dis­closed that his $400 mil­lion Per­sh­ing Square Foun­da­tion, known for its impact invest­ing phi­los­o­phy, has invest­ed cap­i­tal in a com­pa­ny called Cov­axx, which is work­ing to boost anti­body test­ing kits to test peo­ple against the coro­n­avirus dis­ease.

    “We are in one of the most chal­leng­ing peri­ods of time for our coun­try, and for the world. Thou­sands of peo­ple have or will soon become severe­ly sick, and many will die,” added Ack­man about the pan­dem­ic, “This is a tragedy that could have been pre­vent­ed with bet­ter long-term plan­ning, which should have begun more than a decade ago. I have always said that expe­ri­ence is mak­ing mis­takes and learn­ing from them. And learn from this we must.”
    ...

    But also keep in mind that being an investor in a com­pa­ny that’s work­ing to pro­vide one of the key com­po­nents of reopen­ing economies is pos­si­bly going to pro­vide Per­sh­ing Square Cap­i­tal future oppor­tu­ni­ties for mas­sive “out of the mon­ey” bets of this nature. If Cov­axx was to announce soon that it has an approve anti­body test that could be deliv­ered soon at scale, that announce­ment alone would prob­a­bly move the mar­kets dra­mat­i­cal­ly upwards. What kinds of options trad­ing might give 100-fold returns fol­low­ing that kind of announce­ment? We can prob­a­bly be sure some­one at Per­sh­ing Square Cap­i­tal is try­ing to answer that ques­tion.

    So the take away mes­sage from this whole sto­ry is that when we have his­toric mar­ket swings like we’ve seen, mas­sive for­tunes can be made in short order. Some of those mas­sive for­tunes might come from luck, oth­ers from keen fore­sight, and are inevitably going to involve insid­er infor­ma­tion and knowl­edge of key upcom­ing events and poli­cies. It’s a par­tic­u­lar­ly impor­tant aspect of this cri­sis to keep in mind giv­en that we have the ’emol­u­ments claus­es don’t apply to us’ Trump admin­is­tra­tion that’s going to be mak­ing a lot of those key mar­ket-mov­ing deci­sions. What kinds of insights about upcom­ing mar­ket-mov­ing poli­cies might noto­ri­ous short-sell­er J. Kyle Bass receive from his close friend Tom­my Hicks Jr. who just hap­pens to be Don­ald Trump Jr.‘s hunt­ing bud­dy? Who knows, but giv­en that the coro­n­avirus pan­dem­ic was pre­ced­ed by a pan­dem­ic of epic cor­rup­tion with the US rul­ing class that has cul­mi­nat­ed in the pres­i­den­cy of some­one like Don­ald Trump, these are the kinds of ques­tions we unfor­tu­nate­ly need to be ask­ing at the same time we’re ask­ing the basic ques­tion of how to deal with this pan­dem­ic. Mas­sive overnight for­tunes pred­i­cat­ed on insid­er knowl­edge and the craft­ing of sober pan­dem­ic respons­es aren’t a great mix.

    Posted by Pterrafractyl | March 28, 2020, 4:12 pm
  3. Why was the fed­er­al ban on pro­duc­tion of lethal virus­es lift­ed in 2017? https://www.nytimes.com/2017/12/19/health/lethal-viruses-nih.html

    Why was fund­ing to CDC per­son­nel assigned to Chi­na cut in 2018?
    https://mobile.twitter.com/JuddLegum/status/1232051346796371968

    Was there an unusu­al spike in live­stock sales from USDA to Chi­na since ear­ly 2018 cor­re­spond­ing to the begin­ning of the “trade war”?

    Is it pos­si­ble to take a genet­i­cal­ly mod­i­fied virus, then gen­er­a­tional­ly har­vest and mutate “nat­ur­al” genes? https://www.sciencemag.org/news/2011/11/scientists-brace-media-storm-around-controversial-flu-studies#

    Bio­log­i­cal war­fare agents are most­ly invis­i­ble to the human eye and nat­u­ral­ly present in the envi­ron­ment. One of the advan­tages of using bio­log­i­cal war­fare could be “an opti­mal death to cost ratio; they are vir­tu­al­ly unde­tectable; and they offer the poten­tial for mass panic.”56 This is a pos­i­tive moti­va­tion for nations, groups, and indi­vid­u­als to pur­sue genet­i­cal­ly engi­neered pathogens as a weapon of choice. *Bio­log­i­cal war­fare attacks may resem­ble a nat­ur­al dis­ease out­break phe­nom­e­non and it would be very dif­fi­cult to trace back to the source, there­by dis­count­ing the perpetrator’s actions.* BIOTECHNOLOGY: GENETICALLY ENGINEERED PATHOGENS Lt Col Joel Almosara, BSC, USAF June 2010

    Two breech­es of con­tain­ment at Ft. Det­rick. [This could have been a relat­ed ‘warn­ing — some­thing big is com­ing’ type event]
    https://www.military.com/daily-news/2019/11/24/cdc-inspection-findings-reveal-more-about-fort-detrick-research-suspension.html

    Accord­ing to a George­town Uni­ver­si­ty, and Eras­mus Med­ical Cen­ter Uni­ver­si­ty Nether­lands study the virus may have orig­i­nat­ed as ear­ly as 18 Sep­tem­ber 2019 and not of “wet mar­ket” ori­gin.

    Then we have Steve Ban­non’s increas­ing­ly hos­tile regime change rhetoric around this time; and more recent­ly, Bill Gates’ mani­a­cal laugh­ter on CNN. But I’m sure you’ve got that cov­ered.

    Posted by Diana Shore | April 3, 2020, 10:43 pm
  4. https://www.bbc.com/news/world-us-canada-52194018

    Stark sta­tis­tics from Chica­go health offi­cials have under­scored the heavy toll of coro­n­avirus on black Amer­i­cans.

    Black Chicagoans account for half of all coro­n­avirus cas­es in the city and more than 70% of deaths, despite mak­ing up 30% of the pop­u­la­tion.

    Oth­er cities with large black pop­u­la­tions, includ­ing Detroit, Mil­wau­kee, New Orleans and New York, have become coro­n­avirus hotspots.

    The US has record­ed near­ly 370,000 virus cas­es and almost 11,000 deaths.

    Glob­al­ly there have been near­ly 75,000 deaths and more than 1.3m cas­es total.

    What do Chicago’s sta­tis­tics show?
    As of 5 April, 1,824 out of Chicago’s 4,680 con­firmed Covid-19 cas­es were black res­i­dents, said city offi­cials on Mon­day.

    That com­pared with 847 white, 478 His­pan­ic and 126 Asian Chicagoans.

    Chica­go has seen a total of 98 deaths as of Sun­day, with 72% of them black res­i­dents.

    The dis­par­i­ty is reflect­ed across the state, where black peo­ple account for 41% of Covid-19 deaths, despite mak­ing up 14% of the pop­u­la­tion of Illi­nois.

    Chica­go pub­lic health com­mis­sion­er Dr Alli­son Arwady told reporters that black city res­i­dents already lived on aver­age about 8.8 years less than their white coun­ter­parts.

    May­or Lori Light­foot said the coro­n­avirus was “dev­as­tat­ing black Chica­go”.

    She said city inspec­tors would be sent into shops to ensure every­one was adher­ing to social dis­tanc­ing guide­lines.

    May­or Light­foot also raised the pos­si­bil­i­ty of cur­fews in areas where peo­ple gath­ered out­side liquor stores, reports the Chica­go Sun-Times.

    What’s the pic­ture nation­al­ly?

    Though the coro­n­avirus has been called the “great equal­iz­er”, data sug­gests that vul­ner­a­bil­i­ty to the infec­tion may vary by neigh­bour­hood. [ed. note: It’s curi­ous that they use ‘neigh­bor­hood’ while the entire arti­cle focus­es on “race”.]

    In Michi­gan, African Amer­i­cans make up 14% of the pop­u­la­tion, but they account for 33% of the coro­n­avirus cas­es and 41% of deaths, fig­ures from the state health depart­ment showed on Mon­day.

    White res­i­dents account for about 23% of record­ed cas­es in Michi­gan and 28% of deaths, accord­ing to the data.

    Detroit, Michi­gan, is about 80% black, and the city togeth­er with its sur­round­ing sub­urbs accounts for around 80% of con­firmed coro­n­avirus cas­es.

    A sim­i­lar dis­par­i­ty has emerged in Mil­wau­kee, Wis­con­sin, one of the most seg­re­gat­ed cities in the US.

    African Amer­i­cans made up almost half of Mil­wau­kee Coun­try’s near­ly 1,000 cas­es as of last Fri­day and 81% of its 27 deaths, despite black peo­ple account­ing for 26% of the pop­u­la­tion there, accord­ing to a study by ProP­ub­li­ca.

    Some 40% of Louisiana’s coro­n­avirus deaths have occurred in the New Orleans area, where the major­i­ty of res­i­dents are black.

    Health offi­cials have pre­vi­ous­ly said the Big Easy’s res­i­dents suf­fer from rates of obe­si­ty, dia­betes and hyper­ten­sion that are high­er than the nation­al aver­age, mak­ing them more vul­ner­a­ble to Covid-19.

    What’s behind the dis­par­i­ty in Chica­go?

    May­or Light­foot said dia­betes, heart dis­ease and res­pi­ra­to­ry ill­ness were “real­ly preva­lent” in black com­mu­ni­ties.

    Dr Arwady told reporters that even if every­one in the city did have access to a doc­tor, “we would still see sig­nif­i­cant health dis­par­i­ties because of food deserts and lack of walk­a­ble streets”.

    Dr Cameron Webb, an African-Amer­i­can physi­cian who is run­ning for Con­gress in the US state of Vir­ginia, told BBC News that US racial and eco­nom­ic dis­par­i­ties were being ampli­fied by the pan­dem­ic.

    “It real­ly expos­es our soci­ety’s fault lines,” he said.

    Alder­man Jason Ervin, who chairs Chica­go coun­cil’s black cau­cus, told the Chica­go Tri­bune that “rates of non-com­pli­ance in some parts of the city with the stay-at-home orders” might also be con­tribut­ing to the sta­tis­tics.

    Posted by Ovid 19 | April 6, 2020, 7:29 pm
  5. THIS IS WHAT PRESIDENT TOXIC DUMP IS DOING TO DESTROY THE BLUE STATES BY ONLY HELPING ONLY THE RED STATES IN THIS PANDEMIC.

    Hos­pi­tals say feds are seiz­ing masks and oth­er coro­n­avirus sup­plies with­out a word

    https://www.latimes.com/politics/story/2020–04-07/hospitals-washington-seize-coronavirus-supplies

    Posted by Roberto Maldonado | April 8, 2020, 1:29 pm
  6. I want­ed to post this here for any lis­ten­ers who may be inter­est­ed. The short ver­sion is this: Zinc sup­ple­ments may help reg­u­late cytokines and pre­vent the sort of inflam­ma­tion asso­ci­at­ed with the cytokine storm. Also: Zinc has been shown to be effec­tive in ward­ing off the ‘com­mon cold’ which is a type of coro­n­avirus. Don’t know if this is worth any­thing but the source seems legit.- TGWE.

    In ath­er­o­scle­ro­sis and dia­betes mel­li­tus, the con­comi­tant pres­ence of low-grade sys­temic inflam­ma­tion and mild zinc defi­cien­cy high­lights a role for zinc nutri­tion in the man­age­ment of chron­ic dis­ease. This review aims to eval­u­ate the lit­er­a­ture that reports on the inter­ac­tions of zinc and cytokines. In humans, inflam­ma­to­ry cytokines have been shown both to up- and down-reg­u­late the expres­sion of spe­cif­ic cel­lu­lar zinc trans­porters in response to an increased demand for zinc in inflam­ma­to­ry con­di­tions. The acute phase response includes a rapid decline in the plas­ma zinc con­cen­tra­tion as a result of the redis­tri­b­u­tion of zinc into cel­lu­lar com­part­ments. Zinc defi­cien­cy influ­ences the gen­er­a­tion of cytokines, includ­ing IL-1β, IL‑2, IL‑6, and TNF‑α, and in response to zinc sup­ple­men­ta­tion plas­ma cytokines exhib­it a dose-depen­dent response. The mech­a­nism of action may reflect the abil­i­ty of zinc to either induce or inhib­it the acti­va­tion of NF-κB. Con­founders in under­stand­ing the zinc-cytokine rela­tion­ship on the basis of in vit­ro exper­i­men­ta­tion include method­olog­i­cal issues such as the cell type and the means of acti­vat­ing cells in cul­ture. Impaired zinc home­osta­sis and chron­ic inflam­ma­tion fea­ture promi­nent­ly in a num­ber of car­diometa­bol­ic dis­eases. Giv­en the high preva­lence of zinc defi­cien­cy and chron­ic dis­ease glob­al­ly, the inter­play of zinc and inflam­ma­tion war­rants fur­ther exam­i­na­tion.

    Nutri­ents. 2012 Jul; 4(7): 676–694.
    Pub­lished online 2012 Jul 4. doi: 10.3390/nu4070676
    PMCID: PMC3407988
    PMID: 22852057
    Zinc and Reg­u­la­tion of Inflam­ma­to­ry Cytokines: Impli­ca­tions for Car­diometa­bol­ic Dis­ease

    Posted by TGWE | April 8, 2020, 11:58 pm
  7. I thought to post this here, as there is no link to the orig­i­nal arti­cle you ref­er­enced. This is from the Jan­u­ary 22 edi­tion of the Inde­pen­dent:

    https://www.independent.co.uk/news/germ-warfare-could-target-ethnic-groups-1075365.html

    Germ war­fare ‘could tar­get eth­nic groups’
    By Charles Arthur
    Fri­day 22 Jan­u­ary 1999 01:02
    GENETICALLY engi­neered bio­log­i­cal weapons capa­ble of tar­get­ing par­tic­u­lar eth­nic groups could become real­i­ty with­in 10 years, an expert pan­el warned yes­ter­day.

    Virus­es and oth­er micro-organ­isms tai­lored to detect the dif­fer­ences in the DNA of races could offer war­mak­ers and ter­ror­ists of the future a new means to car­ry out “eth­nic cleans­ing”, said the pan­el con­vened by the British Med­ical Asso­ci­a­tion (BMA).

    Yet the sci­en­tif­ic advances that would make such weapons pos­si­ble will be a spin-off of two areas of med­i­cine with poten­tial­ly huge ben­e­fits. The first is the Human Genome Project, which aims to unrav­el the 100,000 or so genes in human DNA by 2003. The oth­er is the nascent tech­nol­o­gy of gene ther­a­py, which tries to repair defec­tive genes in the body.

    Launch­ing a book enti­tled Biotech­nol­o­gy, Weapons and Human­i­ty, mem­bers of the pan­el insist­ed yes­ter­day that they were not scare­mon­ger­ing. “We went into this being very scep­ti­cal, with a posi­tion that ‘It can’t be done’,” said Pro­fes­sor Vivi­enne Nathanson, the BMA’s head of health pol­i­cy and research. “But then after exam­in­ing what is going on we decid­ed that it might be pos­si­ble after all.”

    The idea of “genet­ic weapons”, which the pan­el said are at present just a the­o­ret­i­cal pos­si­bil­i­ty, added urgency to the need to add ver­i­fi­ca­tion pro­ce­dures to the Bio­log­i­cal and Tox­in Weapons Con­ven­tion. Though first signed in 1972 by the UK, US and Rus­sia, and now hav­ing 140 sig­na­to­ry nations, the BWC dif­fers from oth­er weapons con­ven­tions in hav­ing no mech­a­nisms for over­sight, to ensure that sig­na­to­ries obey its rules.

    Rus­sia was among the coun­tries that attempt­ed to pro­duce a genet­i­cal­ly enhanced ver­sion of the anthrax virus dur­ing the Cold War. The Aum Shin­rikyo reli­gious ter­ror­ists in Japan also sought genet­i­cal­ly to enhance bac­te­ria they had acquired, but failed.

    Posted by TGWE | April 9, 2020, 6:26 am
  8. 10,000 Cas­es And 500 Deaths In Africa. Health Offi­cials Say It’s Just The Begin­ning
    April 8, 20206:27 PM ET
    Pien Huang

    Kola Sulaimon/AFP via Get­ty Images
    Coro­n­avirus case counts are ris­ing expo­nen­tial­ly in Africa. Since the con­ti­nent saw its first case, in Egypt in mid-Feb­ru­ary, some 10,000 cas­es and 500 deaths have been con­firmed.

    Pub­lic health offi­cials think this is just the begin­ning, and they wor­ry that the sit­u­a­tion in the com­ing weeks will get much worse. “COVID-19 has the poten­tial not only to cause thou­sands of deaths, but to also unleash eco­nom­ic and social dev­as­ta­tion,” Dr. Mat­shidiso Moeti, WHO region­al direc­tor for Africa, said in a state­ment Wednes­day.

    There are sev­er­al rea­sons why health offi­cials are espe­cial­ly con­cerned about the impact of COVID-19 in African coun­tries.

    First, coun­tries in sub-Saha­ran Africa car­ry some of the world’s heav­i­est bur­dens of seri­ous under­ly­ing con­di­tions such as HIV, which lim­its immune func­tion, and tuber­cu­lo­sis, which often scars the lungs. Mal­nu­tri­tion com­pro­mis­es the health of more than 50 mil­lion chil­dren in the region.

    Then there’s the lim­it­ed access to qual­i­ty care. Num­bers vary by coun­try, but on aver­age across the region, there’s about one doc­tor and five nurs­es for every 5,000 peo­ple. A con­sult with a doc­tor could be far away and pro­hib­i­tive­ly expen­sive.

    And when it comes to spe­cial­ized equip­ment like ven­ti­la­tors that can help severe­ly ill patients breathe, there just aren’t enough of them. “We talk about surg­ing to 75,000 ven­ti­la­tors in New York City, and yet we have whole coun­tries that only have one or two ven­ti­la­tors,” says Joia Mukher­jee, chief med­ical offi­cer for the glob­al health non­prof­it Part­ners in Health.

    “I ful­ly expect that when [COVID-19] hits, if it hits in a big way in impov­er­ished coun­tries, it could have a four to five times high­er mor­tal­i­ty” than in oth­er coun­tries so far, Mukher­jee says.

    In Nige­ria, pub­lic health offi­cials are work­ing to get local man­u­fac­tur­ers to pro­duce var­i­ous types of ven­ti­la­tors, putting up pre­fab­ri­cat­ed iso­la­tion cen­ters and turn­ing hotels and con­ven­tion cen­ters into hos­pi­tal beds. Some 20,000 hos­pi­tal beds will be added to Nige­ri­a’s capac­i­ty by week’s end, says Dr. Adaeze Oreh, a senior offi­cial with the Niger­ian Min­istry of Health.

    The pri­ma­ry strat­e­gy, though, is to try and pre­vent as many infec­tions as pos­si­ble. “We’ve seen the increase in the rates of spread across Africa,” Ore­ah says, “We are try­ing to be proac­tive in try­ing to stop that kind of mas­sive spread in the com­mu­ni­ties.”

    Last week, Nige­ria locked down the cities of Lagos and Abu­ja, telling more than 20 mil­lion res­i­dents to stay at home.

    That’s espe­cial­ly hard in a coun­try where half the pop­u­la­tion is below the pover­ty line, and many peo­ple work every day to earn their dai­ly bread.

    But Nige­ria is bet­ting that the unchecked spread of COVID-19 would be worse.

    https://www.npr.org/sections/coronavirus-live-updates/2020/04/08/830209940/10–000-cases-and-500-deaths-in-africa-health-officials-say-its-just-the-beginnin

    OPINION/CHINA
    A new cold war in Africa
    Increas­ing ten­sions between Chi­na and the US will be detri­men­tal to African pros­per­i­ty and peace.

    Mehari Tad­dele Maru by Mehari Tad­dele Maru
    1 Jul 2019
    https://www.aljazeera.com/indepth/opinion/cold-war-africa-190630102044847.html

    Last week, the 12th US-Africa Busi­ness Sum­mit, a high-lev­el event attend­ed by 11 African heads of state and gov­ern­ment and some 1,000 busi­ness lead­ers, was held in Maputo, Mozam­bique. Dur­ing the three-day event, US offi­cials unveiled a $60bn invest­ment agency which will seek to invest in low and mid­dle-income coun­tries, with a spe­cial focus on Africa.

    The announce­ment came six months after Nation­al Secu­ri­ty Advi­sor John Bolton pre­sent­ed the Trump admin­is­tra­tion’s “New Africa Strat­e­gy”. Accord­ing to the doc­u­ment: “Great pow­er com­peti­tors, name­ly Chi­na and Rus­sia, are rapid­ly expand­ing their finan­cial and polit­i­cal influ­ence across Africa. They are delib­er­ate­ly and aggres­sive­ly tar­get­ing their invest­ments in the region to gain a com­pet­i­tive advan­tage over the Unit­ed States.”

    Although both Chi­na and Rus­sia are men­tioned, over the past few months, the US has demon­strat­ed that it is main­ly con­cerned about the for­mer. In fact, it already appears that Africa is set to become yet anoth­er bat­tle­ground for the esca­lat­ing trade war between Bei­jing and Wash­ing­ton.

    With increas­ing for­eign mil­i­tary pres­ence and grow­ing diplo­mat­ic ten­sions, the con­ti­nent is already wit­ness­ing the first signs of an emerg­ing new cold war. And just like the pre­vi­ous one dev­as­tat­ed Africa, fuelling wars and forc­ing African gov­ern­ments to make eco­nom­ic choic­es not in their best inter­ests, this one will also be detri­men­tal to African devel­op­ment and peace.

    Eco­nom­ic war
    Chi­na’s approach to Africa has always been trade ori­ent­ed. The con­ti­nent became one of the top des­ti­na­tions for Chi­nese invest­ment after Bei­jing intro­duced the so-called “Go Out” pol­i­cy in 1999 which encour­aged pri­vate and state-owned busi­ness to seek eco­nom­ic oppor­tu­ni­ties abroad.

    As a result, Chi­nese trade with Africa has increased 40-fold over the past two decades; in 2017, it stood at $140bn. Between 2003 and 2017, Chi­nese for­eign direct invest­ment (FDI) flows have also jumped more close to 60-fold to $4bn a year; FDI stocks stand at $43bn — a sig­nif­i­cant part of which has gone to infra­struc­ture and ener­gy projects.

    Chi­na has sig­nif­i­cant­ly expand­ed African rail­ways, invest­ing in var­i­ous projects in Kenya, Ethiopia, Dji­bouti, Ango­la and Nige­ria; it is cur­rent­ly build­ing a mas­sive hydropow­er plant in Ango­la and have built Africa’s longest rail­way con­nect­ing Ethiopia and Dji­bouti; it has built the head­quar­ters of the African Union in Addis Aba­ba and the West African region­al bloc ECOWAS in Abu­ja.

    By con­trast, for a long time the US has viewed Africa as a bat­tle­field where it can con­front its ene­mies, whether the Sovi­ets dur­ing the Cold War, ter­ror­ists after 9/11 or now the Chi­nese. Wash­ing­ton has nev­er real­ly made a con­cert­ed effort to devel­op its eco­nom­ic rela­tions with the con­ti­nent.

    As a result, trade between the US and Africa has decreased from $120bn in 2012 to just over $50bn today. US FDI flows have also slumped from $9.4bn in 2009 to around $330m in 2017. The new $60bn invest­ment fund announced last week is a wel­come ini­tia­tive from the US but it will not be able to chal­lenge Chi­nese eco­nom­ic pres­ence on the con­ti­nent. Just last year Chi­nese Pres­i­dent Xi Jin­ping pledged $60bn too but ded­i­cat­ed it sole­ly to invest­ment in Africa.

    The US has repeat­ed­ly accused Chi­na of using “debt to hold states in Africa cap­tive to [its] wish­es and demands” and has warned African states to avoid Chi­nese “debt diplo­ma­cy” which is sup­pos­ed­ly incom­pat­i­ble with the inde­pen­dence of African nations and civ­il soci­ety and pos­es “a sig­nif­i­cant threat to US nation­al secu­ri­ty inter­ests”.

    Yet, Africa is only the fourth-biggest recip­i­ent of Chi­nese FDI after Europe (main­ly Ger­many, UK and Nether­lands), the Amer­i­c­as (main­ly the US and Cana­da), and Asia. The US has also bor­rowed heav­i­ly from Chi­na; cur­rent­ly its debt to its rival stands at $1.12 tril­lion. By con­trast, Africa owes Chi­na around $83bn.

    Africans are ful­ly aware of and con­cerned about high indebt­ed­ness, trade imbal­ances, the rel­a­tive­ly poor qual­i­ty of Chi­nese goods and ser­vices and Bei­jing’s appli­ca­tion of low­er stan­dards of labour and envi­ron­men­tal prac­tices. But many do not share the Amer­i­can per­spec­tive that their eco­nom­ic rela­tion­ship with Chi­na is to their detri­ment and rather see it as an oppor­tu­ni­ty that pro­vides much-need­ed uncon­di­tion­al fund­ing and that takes into account local pri­or­i­ties.

    As Dji­bouti’s Pres­i­dent Ismail Omar Guelleh has point­ed out, “The real­i­ty is that no one but the Chi­nese offers a long-term part­ner­ship.”

    The pres­sure the US is cur­rent­ly exert­ing on African coun­tries to move away from part­ner­ships with Chi­na could hurt African economies. It could force African coun­tries into mak­ing choic­es that are not in their best eco­nom­ic inter­ests and miss out on impor­tant devel­op­ment projects or fund­ing.

    Mean­while, the US-Chi­na trade war is already affect­ing the con­ti­nent. Accord­ing to the African Devel­op­ment Bank, it could cause as much as a 2.5 per­cent decrease in GDP for resource-inten­sive African economies and a 1.9 per­cent dip for oil-export­ing coun­tries.

    Mil­i­tari­sa­tion
    The esca­lat­ing ten­sions between the US and Chi­na could also end up threat­en­ing the secu­ri­ty of the con­ti­nent. Both coun­tries are mil­i­tar­i­ly involved in Africa.

    Over the past 15 years, the Chi­nese Peo­ple’s Lib­er­a­tion Army has been engaged in a num­ber of secu­ri­ty mis­sions across the con­ti­nent, mak­ing mod­est aux­il­iary troop con­tri­bu­tions to peace­keep­ing oper­a­tions in Sudan, South Sudan, Liberia, Mali and the Demo­c­ra­t­ic Repub­lic of Con­go. It has also con­tributed mil­lions of dol­lars of peace­keep­ing equip­ment to the African Union Mis­sion in Soma­lia and pro­vid­ed sig­nif­i­cant fund­ing to the Inter­gov­ern­men­tal Author­i­ty on Devel­op­ment for its medi­a­tion in South Sudan.

    In 2017, the first Chi­nese over­seas mil­i­tary base was opened in Dji­bouti. The facil­i­ty, which cur­rent­ly hosts some 400 staff and troops, and has the capac­i­ty to accom­mo­date 10,000, is offi­cial­ly sup­posed to pro­vide sup­port for the ongo­ing anti-pira­cy oper­a­tions of the Chi­nese navy, but it also plays a role in secur­ing mar­itime routes, part of the Belt and Road Ini­tia­tive. There has also been spec­u­la­tion that this is the first of a num­ber of planned bases meant to secure Chi­nese inter­ests in Africa.

    Chi­na’s mil­i­tary pres­ence in Africa, how­ev­er, pales in com­par­i­son to that of the US. Over the past few years, US Africa Com­mand has run some 36 dif­fer­ent mil­i­tary oper­a­tions in 13 African coun­tries, includ­ing Burk­i­na Faso, Cameroon, Cen­tral African Repub­lic, Chad, Demo­c­ra­t­ic Repub­lic of Con­go, Kenya, Libya, Mali, Mau­ri­ta­nia, Niger, Soma­lia, South Sudan and Tunisia. It has more than 7,000 troops deployed on the con­ti­nent.

    It has a large base in Dji­bouti — the biggest and only per­ma­nent US mil­i­tary base in Africa — but it also runs at least 34 oth­er mil­i­tary out­posts scat­tered across the west, east and north of the con­ti­nent where US troops are deployed and mil­i­tary oper­a­tions (includ­ing drone attacks) are launched from.

    The US also direct­ly sup­ports the armies of Egypt, Nige­ria, Ethiopia, Mali, Niger and oth­ers as well as the G5 Sahel force tasked with coun­tert­er­ror­ism.

    While a direct con­fronta­tion between US and Chi­nese forces in Africa is unlike­ly, their grow­ing pres­ence is becom­ing an increas­ing­ly desta­bil­is­ing fac­tor. Already Wash­ing­ton’s strat­e­gy to con­tain Chi­nese influ­ence over Africa is play­ing out at dif­fer­ent con­flict and social upheaval hotspots across the con­ti­nent. The fall­out of the US-Chi­nese com­pe­ti­tion is par­tic­u­lar­ly appar­ent in the strate­gic Red Sea region, through which pass­es one of the most impor­tant mar­itime routes.

    Coun­tries in the region are not only feel­ing grow­ing US and Chi­nese pres­sure to take one side or the oth­er, but are also increas­ing­ly exposed to out­side inter­fer­ence by var­i­ous region­al pow­ers.

    Grow­ing region­al ten­sions
    Dji­bouti has recent­ly found itself at the cen­tre of US-Chi­nese diplo­mat­ic con­fronta­tion. Being a host to mil­i­tary bases of both super­pow­ers, the small coun­try has had to play a dif­fi­cult bal­anc­ing game.

    In 2018, Dji­bouti seized con­trol of its Doraleh Con­tain­er Ter­mi­nal from the Emi­rati com­pa­ny DP World, claim­ing its oper­a­tion of the facil­i­ty was threat­en­ing its sov­er­eign­ty. The Dji­bouti author­i­ties had feared that the UAE’s invest­ment in the near­by Port of Berbera in the autonomous Soma­li region of Soma­liland could chal­lenge its posi­tion as the main mar­itime hub for Ethiopi­a’s large econ­o­my.

    Its deci­sion to ter­mi­nate the con­tract with DP World, how­ev­er, trig­gered a sharp reac­tion from Wash­ing­ton, a close Emi­rati ally. The Trump admin­is­tra­tion fears that Dji­bouti could hand over con­trol of the ter­mi­nal to Chi­na.

    Bolton has warned: “Should this occur, the bal­ance of pow­er in the Horn of Africa — astride major arter­ies of mar­itime trade between Europe, the Mid­dle East, and South Asia — would shift in favour of Chi­na. And, our US mil­i­tary per­son­nel at Camp Lemon­nier could face even fur­ther chal­lenges in their efforts to pro­tect the Amer­i­can peo­ple.”

    Dji­bouti was forced to declare pub­licly that it would not allow Chi­na to take over the ter­mi­nal but that has not assuaged US fears. Ever since, the US sought to secure a pos­si­ble alter­na­tive loca­tion for its African mil­i­tary base: neigh­bour­ing Eritrea.

    It encour­aged region­al actors, includ­ing Sau­di Ara­bia and the UAE, to pull Eritrea out of its decades-long iso­la­tion. In a mat­ter of months, long-time ene­mies Ethiopia and Eritrea con­clud­ed a peace agree­ment to end their 20-year-old cold con­flict, while the UN lift­ed sanc­tions on Asmara. As a result, Eritrea could emerge as a strate­gic rival to Dji­bouti, offer­ing its coast for for­eign mil­i­tary and eco­nom­ic facil­i­ties. The UAE, for exam­ple, has already set up a mil­i­tary base near the port of Assab.

    Sudan, to the north, has also been the bat­tle­ground of the ongo­ing super­pow­er turf war. Chi­na had been a long-term sup­port­er of Pres­i­dent Omar al-Bashir. Under his rule, Bei­jing came to dom­i­nate its oil indus­try, buy­ing some 80 per­cent of its oil and thus pro­vid­ing Khar­toum with much-need­ed cash to wage war against var­i­ous rebel groups. It was also one of the few coun­tries, along with Rus­sia, that would break the UN arms embar­go and sell weapons to al-Bashir’s regime.

    After South Sudan gained inde­pen­dence in 2011, Chi­na con­tin­ued to be a close part­ner of the Sudanese regime, remain­ing its main trad­ing part­ner. Sudan in fact became the biggest ben­e­fi­cia­ry of the $60bn Africa invest­ment pack­age Chi­na pledged in 2018, hav­ing some $10bn in Chi­nese debt writ­ten off. The Chi­nese gov­ern­ment also made a lot of plans to devel­op facil­i­ties in Port Sudan, where it already oper­ates an oil ter­mi­nal. Qatar and Turkey also signed deals with al-Bashir for var­i­ous facil­i­ties in the port city.

    When mass protests erupt­ed in Decem­ber last year, Bei­jing stood by al-Bashir, who it saw as the main guar­an­tor of sta­bil­i­ty in the coun­try, which falls on strate­gic routes, part of its Belt and Road Ini­tia­tive.

    Mean­while, the US had repeat­ed­ly demon­strat­ed that it did not want al-Bashir run­ning for anoth­er term. His removal was approved in Wash­ing­ton, which has since appeared to back the inter­ests of Sau­di Ara­bia and the UAE in the coun­try.

    The two Gulf states cur­rent­ly hope to install anoth­er strong­man sym­pa­thet­ic to their region­al pol­i­tics, who would main­tain Sudan’s par­tic­i­pa­tion in the war in Yemen and curb Turk­ish and Qatari influ­ence. At this point, it seems Chi­na is at risk of being side­lined by the sig­nif­i­cant sway the UAE and Sau­di Ara­bia have with Sudan’s Tran­si­tion­al Mil­i­tary Coun­cil (TMC).

    Apart from Dji­bouti and Sudan, var­i­ous oth­er coun­tries in the region have felt the con­se­quences of the US bid to con­tain Chi­na. This polit­i­cal con­fronta­tion has also added to the already ris­ing ten­sions between oth­er play­ers in the region, includ­ing Egypt, Gulf coun­tries, Iran and Turkey.

    The Trump admin­is­tra­tion has par­tic­u­lar­ly favoured Emi­rati, Sau­di and Egypt­ian inter­ests which have embold­ened these three coun­tries in their efforts to shape region­al dynam­ics to their advan­tage.

    Thus, in the long-term, giv­en the pre-exist­ing fault­lines and con­flicts in the region, the US-Chi­na cold war could have a detri­men­tal effect, not only on its econ­o­my but also on its secu­ri­ty.

    At this point, to pre­serve its inter­ests and its peace, Africa has only one option: to reject pres­sures to swear alle­giance to either of the two pow­ers. African coun­tries should uphold their sov­er­eign­ty in pol­i­cy and deci­sion-mak­ing and pur­sue the course that is in the best inter­ests of their nations.

    If the US wants to com­pete with Chi­na on the con­ti­nent, it should do so in good faith. It can gain a com­pet­i­tive advan­tage by offer­ing African coun­tries bet­ter, more cred­i­ble and prin­ci­pled alter­na­tives to those put for­ward by Chi­na. But that can only hap­pen if the US devel­ops a strat­e­gy that focus­es on Africa itself, not on con­tain­ing and under­min­ing the busi­ness of a third par­ty.

    The views expressed in this arti­cle are the author’s own and do not nec­es­sar­i­ly reflect Al Jazeer­a’s edi­to­r­i­al stance.

    ABOUT THE AUTHOR
    Mehari Tad­dele Maru Mehari Tad­dele Maru
    Dr Mehari Tad­dele Maru is a schol­ar of peace and secu­ri­ty, law and gov­er­nance, and human rights and migra­tion issues.

    @ drme­hari

    OPINION/CORONAVIRUS PANDEMIC
    Med­ical colo­nial­ism in Africa is not new
    Remarks about test­ing coro­n­avirus drugs on Africans part of pat­tern where some bod­ies are dehu­man­ised, oth­ers pro­tect­ed.

    Karsten Noko by Karsten Noko
    8 Apr 2020
    https://www.aljazeera.com/indepth/opinion/medical-colonialism-africa-200406103819617.html

    Last Wednes­day, a French doc­tor caused con­tro­ver­sy when he pro­posed that vac­cines for the COVID-19 pan­dem­ic be tried on Africans because they lack masks and oth­er per­son­al pro­tec­tive equip­ment.

    By Fri­day, after wide­spread accu­sa­tions of racism, he was forced to apol­o­gise for what he then called his “clum­si­ly expressed” remarks.

    But the type of think­ing exposed by his words is noth­ing new. Nei­ther is it excep­tion­al to this doc­tor. It is part of a trend that for gen­er­a­tions has seen the dehu­man­is­ing of some peo­ple because of the supe­ri­or­i­ty com­plex of oth­ers.

    In ear­ly March 2020, as coro­n­avirus cas­es began an expo­nen­tial growth curve, some peo­ple asked why African coun­tries were not record­ing high­er num­bers of COVID-19 cas­es.

    The tone of these queries had the impact of ques­tion­ing if Africans were some­how genet­i­cal­ly immune to the new virus. But why would this ques­tion even be raised if we know the bio­log­i­cal set-up of all humans is sim­i­lar?

    The dehu­man­i­sa­tion of peo­ple from the Glob­al South was one of the dri­ving forces behind the slave trade and colo­nial­ism. It is incon­ceiv­able that any­one could fath­om the thought of trad­ing in human beings unless they regard­ed that per­son as infe­ri­or.

    Joseph Con­rad, in his book Heart of Dark­ness writ­ing in 1899, grap­pled with the ques­tion of whether the peo­ple he had met in Africa were real­ly human. He opines: “No they were not inhu­man. Well, you know, that was the worst of it — this sus­pi­cion of their not being inhu­man.”

    It is the nat­u­ral­ness of some­one even pos­ing such ques­tions that cements these ideas; the accep­tance of a “sec­ond-class human­i­ty” that allows the dis­pos­ses­sion and trade in human lives to be so eas­i­ly explained away.

    Dehu­man­ised in life, fetishised in death

    Saartjie Baart­man, or Sarah Baart­man as she is com­mon­ly called, was a Khoikhoi woman born in what is present-day South Africa. In 1810, she was abduct­ed and tak­en to Europe where she was turned into an object of an exhi­bi­tion for Euro­pean audi­ences because of her body and her per­ceived large but­tocks.

    Many of the audi­ence mem­bers came to see her because they thought that she was not human. When she died, a French sur­geon dis­sect­ed her body and con­clud­ed that she had ape-like fea­tures.

    In 2002, the South African gov­ern­ment final­ly man­aged to retrieve her body from the French Nation­al Muse­um in Paris where her remains had stood in exhib­it for more than 150 years. Baart­man was dehu­man­ised in life, and fetishised in death, in pur­suit of a sci­en­tif­ic the­o­ry that sought to draw bio­log­i­cal and sci­en­tif­ic dif­fer­ences between white and black peo­ple.

    Two cen­turies after Baartman’s death, the dehu­man­i­sa­tion of cer­tain races is not put on dis­play in such an obvi­ous way. But the trend of using some bod­ies for the ben­e­fit of oth­ers con­tin­ues in dif­fer­ent forms.

    In the 2014 West Africa Ebo­la out­break, for instance, more than 250,000 blood sam­ples were col­lect­ed from patients by lab­o­ra­to­ries in France, the UK and the US among oth­ers — often with no informed con­sent — as patients under­went test­ing and treat­ment for Ebo­la, to help researchers cre­ate new vac­cines and med­i­cines.

    Today, South African, French and Amer­i­can researchers refuse to dis­close how many of these sam­ples they still hold, cit­ing “nation­al secu­ri­ty” as an excuse. As one patient remarked, “They are using it to make research, make bil­lions of dol­lars … That med­i­cine they pro­duce will not be free. It will be some­thing that you will sell.”

    Because the affect­ed com­mu­ni­ties are poor­er and peo­ple lack the infor­ma­tion that will help pro­tect them from such researchers, their sam­ples are tak­en, and used at will to pro­duce med­i­cine for peo­ple who will pay for treat­ment — often with­out their knowl­edge.

    A long his­to­ry of med­ical tri­als
    In 1996, Kano State in Nige­ria was the epi­cen­tre of a huge menin­gi­tis out­break. At the time, Pfiz­er, one of the largest research phar­ma­ceu­ti­cal com­pa­nies in the world, decid­ed to con­duct clin­i­cal tri­als to test a drug it was devel­op­ing.

    Pfiz­er neglect­ed to acquire informed con­sent from the par­ents of the patients, who were, any­way, too stressed to make ratio­nal deci­sions. It was only in 2009 that Pfiz­er set­tled out-of-court and paid $75 mil­lion to the Kano State gov­ern­ment and $175,000 to the par­ents of four of the chil­dren who had died dur­ing the out­break and clin­i­cal tri­als.

    Although Pfiz­er argued in its legal defence that the chil­dren had been killed by the dis­ease and not their drugs, the out-of-court set­tle­ment robbed us of an oppor­tu­ni­ty to have the med­ical facts estab­lished before a court of law.

    Sim­i­lar tri­als and tests were con­duct­ed in Zim­bab­we in 1994 with the drug AZT — projects fund­ed by the US-based CDC and NIH result­ed in adverse effects for patients. In Namib­ia in the ear­ly 1900s, ster­il­i­sa­tion tests were done on Herero women by Ger­man doc­tors who sought to pro­vide “sci­en­tif­ic” back­ing to ban mixed-race mar­riages.

    Researchers know only too well that con­duct­ing such research in the Glob­al North is more oner­ous and has too much red tape. In the Glob­al South, big phar­ma­ceu­ti­cals, often with the com­plic­it sup­port of bribed gov­ern­ment offi­cials, have it easy.

    As they chase huge prof­its, the lives of often unin­formed patients are far from a main con­sid­er­a­tion. For many peo­ple from the affect­ed com­mu­ni­ties, the work of researchers is clear­ly meant to serve the finan­cial inter­ests of those who pre­tend to be kind-heart­ed or phil­an­thropic.

    What remains curi­ous is how dis­eases like TB, malar­ia and hepati­tis con­tin­ue to kill mil­lions every year, and yet the amount of ener­gy and resources being put into erad­i­cat­ing them is nowhere near the efforts against COVID-19 and Ebo­la. It would appear that cer­tain dis­eases get more atten­tion because of the peo­ple they affect or poten­tial­ly threat­en.

    Imag­ined sus­pi­cion?
    In 2011, the CIA, under the cov­er of an inter­na­tion­al NGO, col­lect­ed DNA sam­ples in Pak­istan in a fake vac­ci­na­tion cam­paign as they trailed Osama bin Laden. The move had the impact of strain­ing an already com­pli­cat­ed rela­tion­ship between the US and Pak­istan, but it also had the much wider impact of pro­vid­ing proof to the scep­tics who always sus­pect­ed there was a hid­den agen­da in the deliv­ery of med­ical ser­vices from the Glob­al North.

    In the race to con­tain the coro­n­avirus pan­dem­ic, the last thing over­bur­dened health prac­ti­tion­ers need is some so-called “clum­sy” remarks from a fel­low medic.

    But when a French doc­tor sug­gests that Africa must be includ­ed as part of a vac­cine tri­al, it is not sur­pris­ing that sus­pi­cions and anger are reignit­ed — espe­cial­ly when there are rel­a­tive­ly few­er cas­es on the con­ti­nent than there are in Europe and the US.

    Giv­en the his­to­ry of med­ical colo­nial­ism in Africa, and the cur­rent real­i­ties around the spread of COVID-19, how do we begin to per­suade any­one that those remarks were some­thing oth­er than the con­tin­u­a­tion of a racist, dehu­man­is­ing approach that sees some humans as expend­able?

    How are Africans expect­ed to not react to yet anoth­er attempt to use them as guinea pigs to devel­op drugs that would serve the Glob­al North, whose well-fund­ed health sys­tems can afford the hefty-priced life-sav­ing med­ica­tion that Africans them­selves often die with­out?

    The views expressed in this arti­cle are the author’s own and do not nec­es­sar­i­ly reflect Al Jazeer­a’s edi­to­r­i­al stance.

    ABOUT THE AUTHOR
    Karsten NokoKarsten Noko
    Karsten Noko is a Zim­bab­wean lawyer and human­i­tar­i­an work­ing across sub-Saha­ran Africa.

    @ Karsten­Noko

    Posted by Ovid 19 | April 9, 2020, 10:08 am
  9. Coro­n­avirus destroys lungs. But doc­tors are find­ing its dam­age in kid­neys, hearts and else­where.

    By
    Lenny Bern­stein,
    Car­olyn Y. John­son,
    Sarah Kaplan and
    Lau­rie McGin­ley

    April 15, 2020 at 7:00 AM EDT

    The new coro­n­avirus kills by inflam­ing and clog­ging the tiny air sacs in the lungs, chok­ing off the body’s oxy­gen sup­ply until it shuts down the organs essen­tial for life.

    But clin­i­cians around the world are see­ing evi­dence that sug­gests the virus also may be caus­ing heart inflam­ma­tion, acute kid­ney dis­ease, neu­ro­log­i­cal mal­func­tion, blood clots, intesti­nal dam­age and liv­er prob­lems. That devel­op­ment has com­pli­cat­ed treat­ment for the most severe cas­es of covid-19, the ill­ness caused by the virus, and makes the course of recov­ery less cer­tain, they said.

    The preva­lence of these effects is too great to attribute them sole­ly to the “cytokine storm,” a pow­er­ful immune-sys­tem response that attacks the body, caus­ing severe dam­age, doc­tors and researchers said.

    Almost half the peo­ple hos­pi­tal­ized because of covid-19 have blood or pro­tein in their urine, indi­cat­ing ear­ly dam­age to their kid­neys, said Alan Kliger, a Yale Uni­ver­si­ty School of Med­i­cine nephrol­o­gist who co-chairs a task force assist­ing dial­y­sis patients who have covid-19.

    Even more alarm­ing, he added, is ear­ly data that shows 14 to 30 per­cent of inten­sive-care patients in New York and Wuhan, Chi­na — birth­place of the pan­dem­ic — have lost kid­ney func­tion and require dial­y­sis, or its in-hos­pi­tal cousin, con­tin­u­ous renal replace­ment ther­a­py. New York inten­sive care units are treat­ing so much kid­ney fail­ure, he said, they need more per­son­nel who can per­form dial­y­sis and have issued an urgent call for vol­un­teers from oth­er parts of the coun­try. They also are run­ning dan­ger­ous­ly short of the ster­ile flu­ids used to deliv­er that ther­a­py, he said.

    “That’s a huge num­ber of peo­ple who have this prob­lem. That’s new to me,” Kliger said. “I think it’s very pos­si­ble that the virus attach­es to the kid­ney cells and attacks them.”

    But in med­i­cine, log­i­cal infer­ences often do not prove true when research is con­duct­ed. Every­one inter­viewed for this sto­ry stressed that with the pan­dem­ic still rag­ing, they are spec­u­lat­ing with much less data than is nor­mal­ly need­ed to reach sol­id clin­i­cal con­clu­sions.

    Many oth­er pos­si­ble caus­es for organ and tis­sue dam­age must be inves­ti­gat­ed, they said, includ­ing res­pi­ra­to­ry dis­tress, the med­ica­tions patients received, high fever, the stress of hos­pi­tal­iza­tion in an ICU and the now well-described impact of cytokine storms.

    Still, when researchers in Wuhan con­duct­ed autop­sies on peo­ple who died of covid-19, they found nine of 26 had acute kid­ney injuries and sev­en had par­ti­cles of the coro­n­avirus in their kid­neys, accord­ing to a paper by the Wuhan sci­en­tists pub­lished April 9 in the med­ical jour­nal Kid­ney Inter­na­tion­al.

    “It does raise the very clear sus­pi­cion that at least a part of the acute kid­ney injury that we’re see­ing is result­ing from direct viral involve­ment of the kid­ney, which is dis­tinct from what was seen in the SARS out­break in 2002,” said Paul M. Palevsky, a Uni­ver­si­ty of Pitts­burgh School of Med­i­cine nephrol­o­gist and pres­i­dent-elect of the Nation­al Kid­ney Foun­da­tion.

    One New York hos­pi­tal recent­ly had 51 ICU patients who need­ed 24-hour kid­ney treat­ment but had just 39 machines to do it, he said. The hos­pi­tal had to ration the care, keep­ing each patient on the ther­a­py less than 24 hours a day, he said.

    The virus also may be dam­ag­ing the heart. Clin­i­cians in Chi­na and New York have report­ed myocardi­tis, an inflam­ma­tion of the heart mus­cle, and, more dan­ger­ous, irreg­u­lar heart rhythms that can lead to car­diac arrest in covid-19 patients.

    “They seem to be doing real­ly well as far as res­pi­ra­to­ry sta­tus goes, and then sud­den­ly they devel­op a car­diac issue that seems out of pro­por­tion to their res­pi­ra­to­ry issues,” said Mitchell Elkind, a Colum­bia Uni­ver­si­ty neu­rol­o­gist and pres­i­dent-elect of the Amer­i­can Heart Asso­ci­a­tion. “This seems to be out of pro­por­tion to their lung dis­ease, which makes peo­ple won­der about that direct effect.”

    One review of severe­ly ill patients in Chi­na found that about 40 per­cent suf­fered arrhyth­mias and 20 per­cent had some form of car­diac injury, Elkind said. “There is some con­cern that some of it may be due to direct influ­ence of the virus,” he said.

    The new virus enters the cells of peo­ple who are infect­ed by latch­ing onto the ACE2 recep­tor on cell sur­faces. It unques­tion­ably attacks the cells in the res­pi­ra­to­ry tract, but there is increas­ing sus­pi­cion that it is using the same door­way to enter oth­er cells. The gas­troin­testi­nal tract, for instance, con­tains 100 times more of these recep­tors than oth­er parts of the body, and its sur­face area is enor­mous.

    “If you unfurl it, it’s like a ten­nis court of sur­face area — this tremen­dous area for the virus to invade and repli­cate itself,” said Bren­nan Spiegel, co-edi­tor in chief of the Amer­i­can Jour­nal of Gas­troen­terol­o­gy.

    In a sub­set of covid-19 cas­es, researchers have found, the immune sys­tem bat­tling the infec­tion goes into hyper­drive. The uncon­trolled response leads to the release of a flood of sub­stances called cytokines that, in excess, can result in dam­age to mul­ti­ple organs. In some severe­ly ill covid-19 patients, doc­tors have found high lev­els of a pro-inflam­ma­to­ry cytokine called interleukin‑6, known by the med­ical short­hand IL‑6.

    The unfet­tered response, also called “cytokine release syn­drome,” has long been rec­og­nized in oth­er patients, includ­ing those with autoim­mune dis­eases such as rheuma­toid arthri­tis or in can­cer patients under­go­ing cer­tain immunother­a­pies.

    For covid-19 patients, cytokine storms are a major rea­son that some require inten­sive care and ven­ti­la­tion, said Jef­frey S. Weber, deputy direc­tor of the Perl­mut­ter Can­cer Cen­ter at NYU Lan­gone Med­ical Cen­ter.

    “When your cytokines are sys­tem­i­cal­ly out of con­trol, bad stuff hap­pens,” he said. “It can be a com­plete dis­as­ter.” It isn’t clear why cytokine storms occur in some patients and not oth­ers, though genet­ic fac­tors may play a role, some doc­tors say.

    To treat cytokine storms, some doc­tors are using anti-IL‑6 drugs such as tocilizum­ab, which is approved for can­cer patients who devel­op cytokine storms as a result of immunother­a­py.

    Anoth­er odd, and now well-known, symp­tom of covid-19 is loss of smell and taste. Claire Hop­kins, pres­i­dent of the British Rhi­no­log­i­cal Soci­ety, said stud­ies of patients in Italy and else­where have shown that some lose their sense of smell before they show signs of being sick.

    “The coro­n­avirus can actu­al­ly attack and invade olfac­to­ry nerve end­ings,” Hop­kins said. When these aro­ma-detect­ing fibers are dis­rupt­ed, they can’t send odors to the brain.

    Anos­mia — the med­ical term for the inabil­i­ty to smell — was not ini­tial­ly rec­og­nized as a symp­tom of covid-19, Hop­kins said. Doc­tors were so over­whelmed by patients with severe res­pi­ra­to­ry prob­lems, she said, that “they didn’t ask the ques­tion.”

    But sub­se­quent data from a symp­tom-track­ing app has shown that 60 per­cent of peo­ple lat­er diag­nosed with covid-19 report­ed los­ing their sens­es of smell and taste. About a quar­ter of par­tic­i­pants expe­ri­enced anos­mia before devel­op­ing oth­er symp­toms, sug­gest­ing it can be an ear­ly warn­ing sign of infec­tion.

    Intrigu­ing­ly, Hop­kins said, peo­ple who lose their sense of smell don’t seem to devel­op the same severe res­pi­ra­to­ry prob­lems that have made covid-19 so dead­ly. But a very small num­ber of patients have expe­ri­enced con­fu­sion, low blood oxy­gen lev­els and even lost con­scious­ness — a sign that the virus may have trav­eled along their olfac­to­ry nerve end­ings straight to the cen­tral ner­vous sys­tem.

    “Why you get this dif­fer­ent expres­sion in dif­fer­ent peo­ple, nobody knows,” she said.

    There are also reports that covid-19 can turn people’s eyes red, caus­ing pink­eye, or con­junc­tivi­tis, in some patients. One study of 38 hos­pi­tal­ized patients in Hubei province, Chi­na, found that a third had pink­eye.

    But like many of the non-res­pi­ra­to­ry effects of the virus, this symp­tom may be rel­a­tive­ly uncom­mon — and may devel­op only in peo­ple already severe­ly ill. The fact that the virus has been found in the mucus mem­brane that cov­ers the eye in a small num­ber of patients, how­ev­er, does sug­gest that the eye could be an entry­way for the virus — and is one rea­son that face shields and gog­gles are being used to pro­tect health-care work­ers.

    The virus also is hav­ing a clear impact on the gas­troin­testi­nal tract, caus­ing diar­rhea, vom­it­ing and oth­er symp­toms. One study found that half of covid-19 patients have gas­troin­testi­nal symp­toms, and spe­cial­ists have coined a Twit­ter hash­tag, #NotJust­Cough, to raise aware­ness of them.

    Stud­ies sug­gest that patients with diges­tive symp­toms will also devel­op a cough, but one may occur days before the oth­er.

    “The ques­tion is, is it kind of behav­ing like a hybrid of dif­fer­ent virus­es?” Spiegel said. “What we’re learn­ing is, it seems any­way, that this virus homes in on more than one organ sys­tem.”

    Reports also indi­cate that the virus can attack the liv­er. A 59-year-old woman in Long Island came to the hos­pi­tal with dark urine, which was ulti­mate­ly found to be caused by acute hepati­tis. After she devel­oped a cough, physi­cians attrib­uted the liv­er dam­age to a covid-19 infec­tion.

    Spiegel said he has seen more such reports every day, includ­ing one from Chi­na on five patients with acute viral hepati­tis.

    A par­tic­u­lar dan­ger of the virus appears to be its ten­den­cy to pro­duce blood clots in the veins of the legs and oth­er ves­sels, which can break off, trav­el to the lung and cause death by a con­di­tion known as pul­monary embolism.

    An exam­i­na­tion of 81 patients hos­pi­tal­ized with pneu­mo­nia caused by covid-19 in Wuhan found that 20 had such events and that eight of them died. The peer-reviewed data was pub­lished online April 9 in the Jour­nal of Throm­bo­sis and Hemo­sta­sis.

    Across New York City, blood thin­ners are being used with covid-19 patients much more than expect­ed, said San­jum Sethi, an inter­ven­tion­al car­di­ol­o­gist and assis­tant pro­fes­sor of med­i­cine at Colum­bia University’s Irv­ing Med­ical Cen­ter.

    “We’re just see­ing so many of these events that we have to inves­ti­gate fur­ther,” he said.

    https://www.washingtonpost.com/health/coronavirus-destroys-lungs-but-doctors-are-finding-its-damage-in-kidneys-hearts-and-elsewhere/2020/04/14/7ff71ee0-7db1-11ea-a3ee-13e1ae0a3571_story.html

    Posted by Ovid 19 | April 15, 2020, 8:43 am
  10. AFA #39:
    http://spitfirelist.com/anti-fascist-archives/afa-39-the-world-will-be-plunged-into-an-abyss/
    From the orig­i­nal 1982 ver­sion of “A High­er Form of Killing” is an excerpt from tes­ti­mo­ny before a House appro­pri­a­tions sub­com­mit­tee which said:

    “With­in the next 5 to 10 years, it would prob­a­bly be pos­si­ble to make a new infec­tive micro-organ­ism which could dif­fer in cer­tain impor­tant respects from any known dis­ease-caus­ing organ­isms. Most impor­tant of these is that it might be refrac­to­ry to the immuno­log­i­cal and ther­a­peu­tic process­es upon which we depend to main­tain our rel­a­tive free­dom from infec­tious dis­ease.”

    Peer Reviewed Paper:
    https://www.nature.com/articles/s41423-020‑0424‑9.pdf

    Coro­n­avirus Could Attack Immune Sys­tem Like HIV by Tar­get­ing Pro­tec­tive Cells, Warn Sci­en­tists

    –Researchers in Chi­na and the US find that the virus that caus­es Covid-19 can destroy the T cells that are sup­posed to pro­tect the body from harm­ful invaders
    –One doc­tor said con­cern is grow­ing in med­ical cir­cles that effect could be sim­i­lar to HIV
    “The gene behind the fusion func­tion in Sars-CoV­‑2 was not found in oth­er coro­n­avirus­es in human or ani­mals.”

    April 12, 2020
    https://www.scmp.com/news/china/society/article/3079443/coronavirus-could-target-immune-system-targeting-protective

    The coro­n­avirus that caus­es Covid-19 could kill the pow­er­ful immune cells that are sup­posed to kill the virus instead, sci­en­tists have warned.

    The sur­prise dis­cov­ery, made by a team of researchers from Shang­hai and New York, coin­cid­ed with front­line doc­tors’ obser­va­tion that Covid-19 could attack the human immune sys­tem and cause dam­age sim­i­lar to that found in HIV patients.

    Lu Lu, from Fudan Uni­ver­si­ty in Shang­hai, and Jang Shi­bo, from the New York Blood Cen­tre, joined the liv­ing virus, which is offi­cial­ly known as Sars-CoV­‑2, to lab­o­ra­to­ry-grown T lym­pho­cyte cell lines.

    T lym­pho­cytes, also known as T cells, play a cen­tral role in iden­ti­fy­ing and elim­i­nat­ing alien invaders in the body.

    They do this by cap­tur­ing a cell infect­ed by a virus, bor­ing a hole in its mem­brane and inject­ing tox­ic chem­i­cals into the cell. These chem­i­cals then kill both the virus and infect­ed cell and tear them to pieces.

    To the sur­prise of the sci­en­tists, the T cell became a prey to the coro­n­avirus in their exper­i­ment. They found a unique struc­ture in the virus’ spike pro­tein that appar­ent­ly trig­gered the fusion of a viral enve­lope and cell mem­brane when they came into con­tact.

    The virus’s genes then entered the T cell and took it hostage, dis­abling its func­tion of pro­tect­ing humans.

    The researchers did the same exper­i­ment with severe acute res­pi­ra­to­ry syn­drome, or Sars, anoth­er coro­n­avirus, and found that the Sars virus did not have the abil­i­ty to infect T cells.

    The rea­son, they sus­pect­ed, was the lack of a mem­brane fusion func­tion. Sars, which killed hun­dreds in a 2003 out­break, can only infect cells car­ry­ing a spe­cif­ic recep­tor pro­tein known as ACE2, and this pro­tein has an extreme­ly low pres­ence in T cells.

    Fur­ther inves­ti­ga­tions into the coro­n­avirus infec­tion on pri­ma­ry T cells would evoke “new ideas about path­o­gen­ic mech­a­nisms and ther­a­peu­tic inter­ven­tions”, the researchers said in a paper pub­lished in the peer-reviewed jour­nal Cel­lu­lar & Mol­e­c­u­lar Immunol­o­gy   this week.

    A doc­tor who works in a pub­lic hos­pi­tal treat­ing Covid-19 patients in Bei­jing said the dis­cov­ery added anoth­er piece of evi­dence to a grow­ing con­cern in med­ical cir­cles that the coro­n­avirus could some­times behave like some of the most noto­ri­ous virus­es that direct­ly attack the human immune sys­tem.

    “More and more peo­ple com­pare it to HIV,” said the doc­tor who request­ed not to be named due to the sen­si­tiv­i­ty of the issue.

    In Feb­ru­ary, Chen Yong­wen and his col­leagues at the PLA’s Insti­tute of Immunol­o­gy released a clin­i­cal report warn­ing that the num­ber of T cells could drop sig­nif­i­cant­ly in Covid-19 patients, espe­cial­ly when they were elder­ly or required treat­ment in inten­sive care units. The low­er the T cell count, the high­er the risk of death.

    This obser­va­tion was lat­er con­firmed by autop­sy exam­i­na­tions on more than 20 patients, whose immune sys­tems were almost com­plete­ly destroyed, accord­ing to main­land media reports.

    Doc­tors who had seen the bod­ies said the dam­age to the inter­nal organs was sim­i­lar to a com­bi­na­tion of Sars and Aids.

    The gene behind the fusion func­tion in Sars-CoV­‑2 was not found in oth­er coro­n­avirus­es in human or ani­mals.

    But some dead­ly human virus­es such as Aids and Ebo­la have sim­i­lar sequences, prompt­ing spec­u­la­tion that the nov­el coro­n­avirus might have been spread­ing qui­et­ly in human soci­eties for a long time before caus­ing this pan­dem­ic.

    But there was one major dif­fer­ence between Sars-CoV­‑2 and HIV , accord­ing to the new study. HIV can repli­cate in the T cells and turn them into fac­to­ries to gen­er­ate more copies to infect oth­er cells. But Lu and Jiang did not observe any growth of the coro­n­avirus after it entered the T‑cells, sug­gest­ing that the virus and T‑cells might end up dying togeth­er.

    The study gives rise to some new ques­tions. For instance, the coro­n­avirus can exist for weeks on some patients with­out caus­ing any symp­toms. How it inter­act­ed with the T cells in these patients remained unclear. Some crit­i­cal­ly ill patients also expe­ri­enced cytokine storms, where the immune sys­tem over­re­acts and attacks healthy cells. But why and how the coro­n­avirus trig­gers that effect remains poor­ly under­stood.

    Posted by Mother Muckraker | April 24, 2020, 8:35 pm
  11. @Mother Muck­rak­er–

    Thanks for this! I have heard casu­al dis­cus­sion on not-very-cred­i­ble forums about this dynam­ic, but this is a schol­ar­ly treat­ment.

    Sheeey­it!

    There are many and var­ied symp­toms of infect­ed peo­ple: heart trou­ble, clot­ting, skin rash­es, kid­ney prob­lems in addi­tion to the res­pi­ra­to­ry symp­toms.

    As AIDS cued var­i­ous types of ill­ness by nuk­ing the immune sys­tem, this, too might account for the var­ied immune rea­cions.

    Note a very impor­tant Pter­rafractyl con­tri­bu­tion, not­ing that sig­nif­i­cant num­bers of infect­ed and recov­ered peo­ple showed very lit­tle anti­body pres­ence in their blood­stream.

    That would make the DARPA-fund­ed Mod­er­na Inc.‘s mes­sen­ger RNA vac­cine prob­lem­at­ic at best and worth­less or counter-pro­duc­tive at worst.

    Best,

    Dave

    Posted by Dave Emory | April 26, 2020, 6:33 pm
  12. @Dave and @Mother Muck­rak­er: Regard­ing that pre­vi­ous study out of Chi­na that found the low (or unde­tectable) anti­body lev­els in 30 per­cent of the recov­ered COVID-19 patients they test­ed, it’s worth not­ing that T cells play an impor­tant role in anti­body pro­duc­tion so it would be inter­est­ing to know if the patients with low anti­body counts also had low T cell counts. The study found that the patients with low anti­body lev­els skewed towards the younger patients, prompt­ing the researchers to spec­u­late that their bod­ies were fight­ing off the virus using the non-tar­get­ing parts of the immune sys­tem that don’t involve T‑Cells and anti­bod­ies. They also found that anti­body lev­els rose with age, sug­gest­ing that the bod­ies of the elder­ly were more reliant on the tar­get­ed immune response that uses anti­bod­ies and T cells. So the abil­i­ty of the virus to kill off T cells at the same time younger health­i­er immune sys­tems can defeat the virus with­out rely­ing on T cells might make this virus even more selec­tive­ly dead­ly to the elder­ly and immuno­log­i­cal­ly com­pro­mised than we pre­vi­ous­ly rec­og­nized.

    Now, regard­ing that research that found the virus attacks and kills T cells, it’s also worth not­ing how this find­ing might tie into oth­er stud­ies that have found the virus is capa­ble of infect­ing and dam­ag­ing a large num­ber of organs like the heart, kid­neys, blood ves­sels, but and brain. NOT just the lungs and res­pi­ra­to­ry tract. The researchers who found abil­i­ty to infect T cells also dis­cov­ered was that the virus does­n’t NEED a tar­get cell to have high num­bers of ACE2 recep­tors. The ACE2 recep­tor cer­tain­ly helps because the virus is built to build to that recep­tor but they found cell lines express­ing low lev­els of ACE2 still get­ting infect­ed by SARS-CoV­‑2. And guess what cell types don’t express high lev­els of ACE2: the T cells in their exper­i­ments that were get­ting infect­ed. This led to their spec­u­la­tion that some oth­er recep­tor is play­ing a role in medi­at­ing that mem­brane fusion step. Some oth­er recep­tor that hap­pens to be on the sur­face of T cells. This abil­i­ty to infect cells with­out ACE2 recep­tors appears to be due to anoth­er fea­tures on the virus’s S‑protein...a pro­tein that’s turn­ing out to have a lot of ‘fea­tures’ in this virus!

    Now, it’s worth not­ing that MERS can infect lym­pho­cytes like T cells. MERS is a in the same gen­era as SARS-CoV­‑2 (they’re both Beta coro­n­avirus­es) but a dif­fer­ent lin­eage (MERS is linage C and SARS-CoV­‑2 is B). The orig­i­nal SARS-CoV virus from 2003 — which is the most close­ly relat­ed to SARS-CoV­‑2 genet­i­cal­ly and in the B lin­eage — did not have this fea­ture. A fea­ture that turns out to cru­cial for the virus’s abil­i­ty to attack and kill the part of the immune sys­tem the elder­ly rely on to kill the virus. So SARS-CoV­‑2 would­n’t be unique among human coro­n­avirus­es in this respect but it’s not a fea­ture found in oth­er B lin­eage virus­es (<a href=””>like of like that can­non­i­cal furin cleav­age site on the S‑protein).

    Now, there is a bit of good new all this. As we’ll see in a paper pub­lished by this same research team a week ear­li­er, they’ve been study­ing for year the part of the coro­n­avirus that play a key role in this step in the deliv­ery of the viral RNA pay­load into the cell. After the virus’s S‑protein binds to an ACE2 recep­tor (or per­haps anoth­er mys­tery recep­tor), the pro­tein com­plex con­sist­ing of 6 helices — known as the six-helix bun­dle (6‑HB) — is formed and shifts in its con­for­ma­tion to inter­act with the tar­get cel­l’s mem­ber. The for­ma­tion and con­for­ma­tion­al shift of the 6‑HB bun­dle caus­es a fusion of the viral and cell mem­branes, allow­ing for the depo­si­tion of the viral RNA con­tent in the cell. They’ve been study­ing this process for years and have pre­vi­ous­ly actu­al­ly devel­oped drugs to block the inter­ac­tion of the 6‑HB struc­ture with the tar­get cell mem­brane which stops the repli­ca­tion of the virus. More recent­ly, the team com­pared SARS-CoV-2’s 6‑HB bun­dle to the orig­i­nal SARS-CoV and found three nov­el muta­tions that pre­sum­ably play a role in SARS-CoV-2’s abil­i­ty to fuse with the tar­get cell mem­brane. They then designed a new drug to block this fusion step in SARS-CoV­‑2 and found a poten­tial­ly very potent can­di­date drug. It was a bit of good news amid the avalanche of bad news, although we’ll still pre­sum­ably have to wait years for this drug to go through human clin­i­cal test­ing. But hey, it’s progress.

    First, here’s the let­ter writ­ten by that team to Nature describ­ing their find­ings. Find­ings like an appar­ent abil­i­ty of the virus to infect T cells with­out rely­ing on bind­ing to ACE2 recep­tors first:

    Nature Cel­lu­lar & Mol­e­c­u­lar Immunol­o­gy
    Cor­re­spon­dence

    SARS-CoV­‑2 infects T lym­pho­cytes through its spike pro­tein-medi­at­ed mem­brane fusion

    Xin­ling Wang, Wei Xu, Gaowei Hu, Shuai Xia, Zhip­ing Sun, Zezhong Liu, Youhua Xie, Rong Zhang, Shi­bo Jiang & Lu Lu

    pub­lished 07 April 2020

    COVID-19, the nov­el coro­n­avirus dis­ease caused by SARS-CoV­‑2 and out­bro­ken at the end of 2019 in Wuhan, Chi­na,1 becomes a world­wide pan­dem­ic. SARS-CoV­‑2 belongs to the beta­coro­n­avirus genus and has 79.5% iden­ti­ty to SARS-CoV. SARS-CoV­‑2 uses angiotensin-con­vert­ing enzyme 2 (ACE2) as its host entry recep­tor.2 The clin­i­cal man­i­fes­ta­tions of COVID-19 include pneu­mo­nia, diar­rhea, dys­p­nea, and mul­ti­ple organ fail­ure. Inter­est­ing­ly, lym­pho­cy­tope­nia, as a diag­nos­tic indi­ca­tor, is com­mon in COVID-19 patients. Xiong et al. found upreg­u­la­tion of apop­to­sis, autophagy, and p53 path­ways in PBMC of COVID-19 patients.3 Some stud­ies report­ed that lym­pho­cy­tope­nia might be relat­ed to mor­tal­i­ty, espe­cial­ly in patients with low lev­els of CD3+, CD4+, and CD8+ T lym­pho­cytes.4,5 Lym­pho­cy­tope­nia was also found in the Mid­dle East res­pi­ra­to­ry syn­drome (MERS) cas­es. MERS-CoV can direct­ly infect human pri­ma­ry T lym­pho­cytes and induce T‑cell apop­to­sis through extrin­sic and intrin­sic apop­to­sis path­ways, but it can­not repli­cate in T lym­pho­cytes.6 How­ev­er, it is unclear whether SARS-CoV­‑2 can also infect T cells, result­ing in lym­pho­cy­tope­nia.

    To address this ques­tion, we eval­u­at­ed the sus­cep­ti­bil­i­ty of T lym­pho­cytes to SARS-CoV­‑2 infec­tion. To accom­plish this, pseudo­typed SARS-CoV and SARS-CoV­‑2 were pack­aged based on meth­ods described pre­vi­ous­ly.7 The pseudovirus­es could infect per­mis­sive cells (293T/ACE2 and Huh7 cells) express­ing the ACE2 recep­tor, but could not infect non­per­mis­sive cells (HeLa cells) (Fig. 11a). We used pseudovirus with equal infec­tiv­i­ty to 293T/ACE2 cells (Fig. 11c) to infect two T lym­pho­cyte cell lines, MT‑2 and A3.01, with very low, or close to neg­a­tive, expres­sion lev­el of hACE2 mRNA (Fig. 11b). Sur­pris­ing­ly, over sev­er­al repli­cates, we saw that the T‑cell lines were sig­nif­i­cant­ly more sen­si­tive to SARS-CoV­‑2 infec­tion when com­pared with SARS-CoV (Fig. 11c). In oth­er words, these results tell us that T lym­pho­cytes may be more per­mis­sive to SARS-CoV­‑2 infec­tion and less per­mis­sive for SARS-CoV infec­tion, sim­i­lar to the find­ings in a pre­vi­ous study.6 There­fore, it is plau­si­ble that the S pro­tein of SARS-CoV­‑2 might medi­ate potent infec­tiv­i­ty, even on cells express­ing low hACE2, which would, in turn, explain why the trans­mis­sion rate of SARS-CoV­‑2 is so high. It is also pos­si­ble that oth­er recep­tors medi­ate the entry of SARS-CoV­‑2 into T cells, such as CD147, present on the sur­face of T lymo­ho­cytes,8 which was recent­ly report­ed to be a nov­el inva­sive route for SARS-CoV­‑2.9

    To assess if SARS-CoV­‑2 enters T lym­pho­cytes through non-recep­tor-medi­at­ed endo­cy­to­sis, we used EK1 pep­tide which has been shown to inhib­it SARS-CoV­‑2 spike pro­tein (S) medi­at­ed cell–cell fusion and pseudovirus infec­tion.7,10 Specif­i­cal­ly, it inhibits recep­tor-medi­at­ed infec­tion by inter­act­ing with HR1 to block the for­ma­tion of the six-helix bun­dle (6‑HB), fur­ther inhibit­ing fusion between viral and tar­get cell mem­branes. We found that the EK1 pep­tide had sig­nif­i­cant inhibito­ry activ­i­ty against SARS-CoV­‑2 pseudovirus­es on MT‑2 cells (Fig. 1d), sug­gest­ing that virus entry depends on recep­tor-medi­at­ed fusion. How­ev­er, only a high con­cen­tra­tion (40 µM) of EK1 had inhibito­ry activ­i­ty on MT‑2 cells. Mean­while, the IC50 val­ue of EK1 was 2.38 µM on 293T/ACE2 cells.10 These results sug­gest that SARS-CoV­‑2 can also enter T lym­pho­cytes through the recep­tor-medi­at­ed endo­cy­to­sis path­way. To clar­i­fy, we per­formed a SARS-CoV­‑2 S‑mediated cell–cell fusion assay accord­ing to pre­vi­ous stud­ies.7,10 After 48 h of cocul­ture, 293T cells express­ing SARS-CoV­‑2 S pro­tein fused with MT‑2 cells. Com­pared with unfused cells, the fused cells clus­tered togeth­er and appeared as a large faint green flu­o­res­cent mass. In con­trast, no fused cells were found in the SARS-CoV cocul­ture (Fig. 1e). There­fore, it can be con­clud­ed that SARS-CoV­‑2 might infect T cells through S pro­tein-medi­at­ed mem­brane fusion.

    To fur­ther deter­mine the sus­cep­ti­bil­i­ty of MT‑2 cells to live virus, we used SARS-CoV­‑2 to infect MT‑2 cells and detect­ed the SARS-CoV­‑2 nucle­o­pro­tein (NP) in the cells as report­ed pre­vi­ous­ly.6 Notably, sev­er­al MT‑2 cells were infect­ed with SARS-CoV­‑2 (Fig. 1f). Quan­ti­ta­tive­ly, the per­cent­age of SARS-CoV­‑2 NP-pos­i­tive MT‑2 cells was 23.11% high­er than that of unin­fect­ed cells at 24 h post infec­tion, which is about 4.6‑fold of the por­tion at 1 h (Fig. 1f). This result means that the virus pen­e­trat­ed MT‑2 cells at 24 h and infect­ed them.

    Giv­en that MERS-CoV can effi­cient­ly infect, but not repli­cate, in T lym­pho­cytes,6 we fur­ther detect­ed the num­ber of viral genome copies at dif­fer­ent time points post infec­tion to explore the repli­ca­tion char­ac­ter­is­tics of SARS-CoV­‑2 in MT‑2 cells. Sim­i­lar to MERS-CoV, SARS-CoV­‑2 failed to repli­cate in MT‑2 cells (Fig. 1g). The num­ber of viral genome copies at 6 h was sig­nif­i­cant­ly high­er than oth­er time points in the cell lysate, but always remained steady at all time points in the super­natants. These results sug­gest that SARS-CoV­‑2 may enter MT‑2 cells at 6 h post infec­tion, but does not repli­cate, and then the viral RNA degrade. In super­natants, the detect­ed viral copies might be the back­ground of the resid­ual viri­ons, sim­i­lar to the results of the pre­vi­ous MERS-CoV study (Fig. 1g).6

    Based on the results of pseudovirus and live virus infec­tion, here we proved that (1) SARS-CoV­‑2 could infect T cells, (2) SARS-CoV­‑2 infect­ed T cells through recep­tor-depen­dent, S pro­tein-medi­at­ed mem­brane fusion, and (3) infec­tion could be inhib­it­ed by EK1 pep­tide. How­ev­er, we observed a very low expres­sion lev­el of hACE2 in T cells; there­fore, we fur­ther pro­posed that a nov­el recep­tor might medi­ate SARS-CoV­‑2 entry into T cells. Sim­i­lar to MERS-CoV, SARS-CoV­‑2 infec­tion of T cells is abortive. A recent study report­ed that viral reads bare­ly dis­played in PBMC sam­ples from COVID-19 patients through tran­scrip­tome sequenc­ing of RNAs. Thus, it was inferred that SARS-CoV­‑2 could not infect PBM­Cs. How­ev­er, the tran­scrip­tom­ic char­ac­ter­is­tics of PBM­Cs were detect­ed and ana­lyzed from three patients. Two SARS-CoV­‑2 reads were detect­ed in one patient’s PBM­Cs, and zero reads in anoth­er.3 This result could be attrib­uted to non­pro­duc­tive repli­ca­tion of SARS-CoV­‑2 in T lym­pho­cytes, with lit­tle viral genome in PBM­Cs pos­si­bly degrad­ing in the sam­ple col­lec­tion and RNA extrac­tion process. Thus, the ques­tions of SARS-CoV­‑2 infec­tion and repli­ca­tion in pri­ma­ry T cells and whether the infec­tion induces apop­to­sis in T cells still need fur­ther research, poten­tial­ly evok­ing new ideas about path­o­gen­ic mech­a­nisms and ther­a­peu­tic inter­ven­tions.

    ...

    ————

    “SARS-CoV­‑2 infects T lym­pho­cytes through its spike pro­tein-medi­at­ed mem­brane fusion” by Xin­ling Wang, Wei Xu, Gaowei Hu, Shuai Xia, Zhip­ing Sun, Zezhong Liu, Youhua Xie, Rong Zhang, Shi­bo Jiang & Lu Lu; Nature Cel­lu­lar & Mol­e­c­u­lar Immunol­o­gy; 04/07/2020

    “To assess if SARS-CoV­‑2 enters T lym­pho­cytes through non-recep­tor-medi­at­ed endo­cy­to­sis, we used EK1 pep­tide which has been shown to inhib­it SARS-CoV­‑2 spike pro­tein (S) medi­at­ed cell–cell fusion and pseudovirus infec­tion.7,10 Specif­i­cal­ly, it inhibits recep­tor-medi­at­ed infec­tion by inter­act­ing with HR1 to block the for­ma­tion of the six-helix bun­dle (6‑HB), fur­ther inhibit­ing fusion between viral and tar­get cell mem­branes. We found that the EK1 pep­tide had sig­nif­i­cant inhibito­ry activ­i­ty against SARS-CoV­‑2 pseudovirus­es on MT‑2 cells (Fig. 1d), sug­gest­ing that virus entry depends on recep­tor-medi­at­ed fusion. How­ev­er, only a high con­cen­tra­tion (40 µM) of EK1 had inhibito­ry activ­i­ty on MT‑2 cells. Mean­while, the IC50 val­ue of EK1 was 2.38 µM on 293T/ACE2 cells.10 These results sug­gest that SARS-CoV­‑2 can also enter T lym­pho­cytes through the recep­tor-medi­at­ed endo­cy­to­sis path­way. To clar­i­fy, we per­formed a SARS-CoV­‑2 S‑mediated cell–cell fusion assay accord­ing to pre­vi­ous stud­ies.7,10 After 48 h of cocul­ture, 293T cells express­ing SARS-CoV­‑2 S pro­tein fused with MT‑2 cells. Com­pared with unfused cells, the fused cells clus­tered togeth­er and appeared as a large faint green flu­o­res­cent mass. In con­trast, no fused cells were found in the SARS-CoV cocul­ture (Fig. 1e). There­fore, it can be con­clud­ed that SARS-CoV­‑2 might infect T cells through S pro­tein-medi­at­ed mem­brane fusion.

    It’s the ‘lit­tle S‑protein that could’. We’ve already learned about the S‑protein’s can­non­i­cal furin-cleav­age site that makes it extra easy for the virus to get acti­vat­ed after attach­ing to a cell not found in its clos­est viral rel­a­tives. And now we’re learn­ing that the S‑protein has fea­tures that appear to allow it to infect cells that don’t even have ACE2 recep­tors. Cells like T cells.

    For­tu­nate­ly, there’s one fea­tures this virus does­n’t have (yet): it can infect T cells but can’t repli­cate in them like HIV. This was also found with MERS, a human coro­n­avirus that is in the same gen­era as SARS-CoV­‑2 (they’re both Beta coro­n­avirus­es) but a dif­fer­ent lin­eage (SARS-CoV­‑2 is in the B lin­eage, MERS is in C). Recall how SARS-CoV-2’s furin cleav­age site has nev­er been seen in oth­er B lin­eage Beta coro­n­avirus­es. So this abil­i­ty to infect T cells via this enhanced inter­ac­tion with tar­get cell mem­brane is anoth­er exam­ple of a fea­ture that’s found in oth­er coro­n­avirus­es but not found in oth­er B lin­eage Beta coro­n­avirus­es. It’s like SARS-CoV­‑2 got all the ‘best’ fea­tures from its more dis­tant coro­n­avirus cousins:

    ...
    Giv­en that MERS-CoV can effi­cient­ly infect, but not repli­cate, in T lym­pho­cytes,6 we fur­ther detect­ed the num­ber of viral genome copies at dif­fer­ent time points post infec­tion to explore the repli­ca­tion char­ac­ter­is­tics of SARS-CoV­‑2 in MT‑2 cells. Sim­i­lar to MERS-CoV, SARS-CoV­‑2 failed to repli­cate in MT‑2 cells (Fig. 1g). The num­ber of viral genome copies at 6 h was sig­nif­i­cant­ly high­er than oth­er time points in the cell lysate, but always remained steady at all time points in the super­natants. These results sug­gest that SARS-CoV­‑2 may enter MT‑2 cells at 6 h post infec­tion, but does not repli­cate, and then the viral RNA degrade. In super­natants, the detect­ed viral copies might be the back­ground of the resid­ual viri­ons, sim­i­lar to the results of the pre­vi­ous MERS-CoV study (Fig. 1g).6

    Based on the results of pseudovirus and live virus infec­tion, here we proved that (1) SARS-CoV­‑2 could infect T cells, (2) SARS-CoV­‑2 infect­ed T cells through recep­tor-depen­dent, S pro­tein-medi­at­ed mem­brane fusion, and (3) infec­tion could be inhib­it­ed by EK1 pep­tide. How­ev­er, we observed a very low expres­sion lev­el of hACE2 in T cells; there­fore, we fur­ther pro­posed that a nov­el recep­tor might medi­ate SARS-CoV­‑2 entry into T cells. Sim­i­lar to MERS-CoV, SARS-CoV­‑2 infec­tion of T cells is abortive. A recent study report­ed that viral reads bare­ly dis­played in PBMC sam­ples from COVID-19 patients through tran­scrip­tome sequenc­ing of RNAs. Thus, it was inferred that SARS-CoV­‑2 could not infect PBM­Cs. How­ev­er, the tran­scrip­tom­ic char­ac­ter­is­tics of PBM­Cs were detect­ed and ana­lyzed from three patients. Two SARS-CoV­‑2 reads were detect­ed in one patient’s PBM­Cs, and zero reads in anoth­er.3 This result could be attrib­uted to non­pro­duc­tive repli­ca­tion of SARS-CoV­‑2 in T lym­pho­cytes, with lit­tle viral genome in PBM­Cs pos­si­bly degrad­ing in the sam­ple col­lec­tion and RNA extrac­tion process. Thus, the ques­tions of SARS-CoV­‑2 infec­tion and repli­ca­tion in pri­ma­ry T cells and whether the infec­tion induces apop­to­sis in T cells still need fur­ther research, poten­tial­ly evok­ing new ideas about path­o­gen­ic mech­a­nisms and ther­a­peu­tic inter­ven­tions.
    ...

    Find­ing out the iden­ti­fy of that nov­el cell recep­tor that might medi­ate entry into the T cells. Let’s hope that recep­tor isn’t being expressed by a lot of oth­er tis­sues because those tis­sues will poten­tial­ly be viral tar­gets too.

    Ok, now here’s a paper pub­lished by the same team a week before the above let­ter to nature where they describe their pre­vi­ous work design­ing drugs to block this viral-cell mem­brane fusion step. That drug, EK1, is the same drug they used in the above study to estab­lish that mem­brane fusion was indeed required for the mys­te­ri­ous infec­tions of T cells. The study also men­tions they found three nov­el muta­tions in SARS-CoV­‑2 in one part of its 6‑HB com­plex that car­ries out mem­brane fusion step. Those muta­tions are pre­sum­ably play­ing a role in the abil­i­ty to infect T cells. Final­ly, they men­tion their suc­cess in design­ing a new drug based on EK1 that is far more effec­tive at block­ing the mem­brane fusion step not just on SARS-CoV­‑2 but oth­er human coro­n­avirus­es. So it’s actu­al­ly a poten­tial­ly excit­ing devel­op­ment in terms of the quest for an effec­tive drug.

    They men­tion that the Recep­tor Bind­ing Domain (RBD) of the S‑protein of SARS-CoV­‑2 has a 10-to-20 fold greater affin­i­ty to bind­ing to the ACE2 recep­tor on the tar­get cells than the orig­i­nal SARS-CoV. It’s one of the oth­er ‘fea­tures’ of this virus’s S‑protein. So SARS-CoV­‑2 is not only extra good at bind­ing to ACE2 recep­tors (then then get­ting acti­vat­ed by the furin cleav­age-site after bind­ing) but it’s also adept at enter­ing cells with­out rely­ing on ACE2 recep­tors:

    Nature Cell Research

    Inhi­bi­tion of SARS-CoV­‑2 (pre­vi­ous­ly 2019-nCoV) infec­tion by a high­ly potent pan-coro­n­avirus fusion inhibitor tar­get­ing its spike pro­tein that har­bors a high capac­i­ty to medi­ate mem­brane fusion

    Shuai Xia, Meiqin Liu, Chao Wang, Wei Xu, Qiaoshuai Lan, Sil­iang Feng, Feifei Qi, Lin­lin Bao, Lany­ing Du, Shuwen Liu, Chuan Qin, Fei Sun, Zhengli Shi, Yun Zhu, Shi­bo Jiang & Lu Lu

    vol­ume 30, pages343–355(2020)
    Pub­lished: 30 March 2020

    Abstract

    The recent out­break of coro­n­avirus dis­ease (COVID-19) caused by SARS-CoV­‑2 infec­tion in Wuhan, Chi­na has posed a seri­ous threat to glob­al pub­lic health. To devel­op spe­cif­ic anti-coro­n­avirus ther­a­peu­tics and pro­phy­lac­tics, the mol­e­c­u­lar mech­a­nism that under­lies viral infec­tion must first be defined. There­fore, we here­in estab­lished a SARS-CoV­‑2 spike (S) pro­tein-medi­at­ed cell–cell fusion assay and found that SARS-CoV­‑2 showed a supe­ri­or plas­ma mem­brane fusion capac­i­ty com­pared to that of SARS-CoV. We solved the X‑ray crys­tal struc­ture of six-heli­cal bun­dle (6‑HB) core of the HR1 and HR2 domains in the SARS-CoV­‑2 S pro­tein S2 sub­unit, reveal­ing that sev­er­al mutat­ed amino acid residues in the HR1 domain may be asso­ci­at­ed with enhanced inter­ac­tions with the HR2 domain. We pre­vi­ous­ly devel­oped a pan-coro­n­avirus fusion inhibitor, EK1, which tar­get­ed the HR1 domain and could inhib­it infec­tion by diver­gent human coro­n­avirus­es test­ed, includ­ing SARS-CoV and MERS-CoV. Here we gen­er­at­ed a series of lipopep­tides derived from EK1 and found that EK1C4 was the most potent fusion inhibitor against SARS-CoV­‑2 S pro­tein-medi­at­ed mem­brane fusion and pseudovirus infec­tion with IC50s of 1.3 and 15.8 nM, about 241- and 149-fold more potent than the orig­i­nal EK1 pep­tide, respec­tive­ly. EK1C4 was also high­ly effec­tive against mem­brane fusion and infec­tion of oth­er human coro­n­avirus pseudovirus­es test­ed, includ­ing SARS-CoV and MERS-CoV, as well as SARSr-CoVs, and potent­ly inhib­it­ed the repli­ca­tion of 5 live human coro­n­avirus­es exam­ined, includ­ing SARS-CoV­‑2. Intranasal appli­ca­tion of EK1C4 before or after chal­lenge with HCoV-OC43 pro­tect­ed mice from infec­tion, sug­gest­ing that EK1C4 could be used for pre­ven­tion and treat­ment of infec­tion by the cur­rent­ly cir­cu­lat­ing SARS-CoV­‑2 and oth­er emerg­ing SARSr-CoVs.

    Intro­duc­tion

    In April of 2018, the World Health Orga­ni­za­tion (WHO) estab­lished a pri­or­i­ty list of pathogens, includ­ing Mid­dle East res­pi­ra­to­ry syn­drome (MERS), severe acute res­pi­ra­to­ry syn­drome (SARS) and Dis­ease X, a dis­ease with an epi­dem­ic or pan­dem­ic poten­tial caused by an unknown pathogen1,2 (Fig. 1a).

    In late Decem­ber 2019, an out­break of pneu­mo­nia with an unknown eti­ol­o­gy in Wuhan, Chi­na was con­sid­ered as the first Dis­ease X fol­low­ing the announce­ment by WHO. Short­ly there­after, a nov­el coro­n­avirus, 2019-nCoV, as denot­ed by WHO,3 was iden­ti­fied as the pathogen caus­ing the coro­n­avirus dis­ease COVID-19.4,5 2019-nCoV with 79.5 and 96% sequence iden­ti­ty to SARS-CoV and a bat coro­n­avirus, SL-CoV-RaT­G13, respec­tive­ly,6 was renamed SARS-CoV­‑2 by the Coro­n­aviri­dae Study Group (CSG) of the Inter­na­tion­al Com­mit­tee on Tax­on­o­my of Virus­es (ICTV),7 while, in the inter­im, it was renamed HCoV-19, as a com­mon virus name, by a group of virol­o­gists in Chi­na.8,9,10

    As of 24 Feb­ru­ary 2020, a total of 79,331 con­firmed cas­es of COVID-19, includ­ing 2618 deaths, were report­ed in Chi­na and 27 oth­er coun­tries,11 pos­ing a seri­ous threat to glob­al pub­lic health and thus call­ing for the prompt devel­op­ment of spe­cif­ic anti-coro­n­avirus ther­a­peu­tics and pro­phy­lac­tics for treat­ment and pre­ven­tion of COVID-19.

    Coro­n­avirus­es (CoVs), the largest RNA virus­es iden­ti­fied so far, belong­ing to the Coro­n­aviri­dae fam­i­ly, are divid­ed into 4 gen­era, a‑, ß‑, d- and γ‑coronaviruses, while the ß‑coronaviruses are fur­ther divid­ed into A, B, C, and D lin­eages. The sev­en CoVs that can infect humans (HCoVs) include HCoV-229E and HCoV-NL63 in the a‑coronaviruses, HCoV-OC43 and HCoV-HKU1 in the ß‑coronaviruses lin­eage A, SARS-CoV and SARS-CoV­‑2 in the ß‑coronaviruses lin­eage B (ß‑B coro­n­avirus­es), and MERS-CoV in the ß‑coronaviruses lin­eage C.6 To devel­op spe­cif­ic SARS-CoV­‑2 fusion inhibitors, it is essen­tial to study the fusion capac­i­ty of SARS-CoV­‑2 com­pared to that of SARS-CoV. Par­tic­u­lar­ly, SARS-CoV and SARS-CoV­‑2 have 89.8% sequence iden­ti­ty in their spike (S) pro­teins S2 sub­units, which medi­ate the mem­brane fusion process, and both of their S1 sub­units uti­lize human angiotensin-con­vert­ing enzyme 2 (hACE2) as the recep­tor to infect human cells.6 Most impor­tant­ly, the ACE2-bind­ing affin­i­ty of the recep­tor-bind­ing domain (RBD) in S1 sub­unit of S pro­tein of SARS-CoV­‑2 is 10- to 20-fold high­er than that of SARS-CoV,12 which may con­tribute to the high­er infec­tiv­i­ty and trans­mis­si­bil­i­ty of SARS-CoV­‑2 com­pared to SARS-CoV. How­ev­er, it is unclear whether SARS-CoV­‑2 can medi­ate mem­brane fusion in a man­ner that exceeds the capac­i­ty of SARS-CoV.

    After bind­ing of RBD in S1 sub­unit of S pro­tein on the viri­on to the ACE2 recep­tor on the tar­get cell, the hep­tad repeat 1 (HR1) and 2 (HR2) domains in its S2 sub­unit of S pro­tein inter­act with each oth­er to form a six-helix bun­dle (6‑HB) fusion core, bring­ing viral and cel­lu­lar mem­branes into close prox­im­i­ty for fusion and infec­tion.13 There­fore, the 6‑HB fusion core struc­ture of SARS-CoV­‑2 and SARS-CoV S pro­teins should also be com­pared in order to inves­ti­gate the struc­tur­al basis for mem­brane fusion medi­at­ed by their S pro­teins and thus set the stage for the ratio­nal design of coro­n­avirus fusion inhibitors.

    In our pre­vi­ous stud­ies, we designed a pan-coro­n­avirus fusion inhibitor, EK1, tar­get­ing the HR1 domains of HCoV S pro­teins, which proved to be effec­tive in inhibit­ing infec­tion of 5 HCoVs, includ­ing SARS-CoV and MERS-CoV, and 3 SARS-relat­ed CoVs (SARSr-CoVs). By intranasal appli­ca­tion of this pep­tide, either pre- or post-chal­lenge with coro­n­avirus, the treat­ed mice were pro­tect­ed from HCoV-OC43 or MERS-CoV infec­tion, sug­gest­ing that this pep­tide has pro­phy­lac­tic and ther­a­peu­tic poten­tial against SARS-CoV­‑2 infec­tion.14 Indeed, our recent stud­ies have shown that EK1 pep­tide is effec­tive against SARS-CoV­‑2 S pro­tein-medi­at­ed mem­brane fusion and PsV infec­tion in a dose-depen­dent man­ner.15

    In this study, we have shown that SARS-CoV­‑2 exhibits much high­er capac­i­ty of mem­brane fusion than SARS-CoV, sug­gest­ing that the fusion machin­ery of SARS-CoV­‑2 is an impor­tant tar­get for devel­op­ment of coro­n­avirus fusion inhibitors. We have solved the X‑ray crys­tal struc­ture of SARS-CoV‑2’s 6‑HB core and iden­ti­fied sev­er­al mutat­ed amino acid residues in HR1 domain respon­si­ble for its enhanced inter­ac­tions with HR2 domain. By con­ju­gat­ing the cho­les­terol mol­e­cule to the EK1 pep­tide, we found that one of the lipopep­tides, EK1C4, exhib­it­ed high­ly potent inhibito­ry activ­i­ty against SARS-CoV­‑2 S‑mediated mem­brane fusion and PsV infec­tion, about 240- and 150-fold more potent than EK1 pep­tide, respec­tive­ly. EK1C4 is also high­ly effec­tive against in vit­ro and in vivo infec­tion of some live HCoVs, such as SARS-CoV­‑2, HCoV-OC43 and MERS-CoV, sug­gest­ing poten­tial for fur­ther devel­op­ment as pan-CoV fusion inhibitor-based ther­a­peu­tics and pro­phy­lac­tics for treat­ment and pre­ven­tion of infec­tion by the cur­rent­ly cir­cu­lat­ing SARS-CoV­‑2 and MERS-CoV, as well as future reemerg­ing SARS-CoV and emerg­ing SARSr-CoVs.

    ...

    ———–

    “Inhi­bi­tion of SARS-CoV­‑2 (pre­vi­ous­ly 2019-nCoV) infec­tion by a high­ly potent pan-coro­n­avirus fusion inhibitor tar­get­ing its spike pro­tein that har­bors a high capac­i­ty to medi­ate mem­brane fusion” by Shuai Xia, et al; Nature Cell Research; Pub­lished: 30 March 2020(2020)volume 30, pages343–355

    “The recent out­break of coro­n­avirus dis­ease (COVID-19) caused by SARS-CoV­‑2 infec­tion in Wuhan, Chi­na has posed a seri­ous threat to glob­al pub­lic health. To devel­op spe­cif­ic anti-coro­n­avirus ther­a­peu­tics and pro­phy­lac­tics, the mol­e­c­u­lar mech­a­nism that under­lies viral infec­tion must first be defined. There­fore, we here­in estab­lished a SARS-CoV­‑2 spike (S) pro­tein-medi­at­ed cell–cell fusion assay and found that SARS-CoV­‑2 showed a supe­ri­or plas­ma mem­brane fusion capac­i­ty com­pared to that of SARS-CoV. We solved the X‑ray crys­tal struc­ture of six-heli­cal bun­dle (6‑HB) core of the HR1 and HR2 domains in the SARS-CoV­‑2 S pro­tein S2 sub­unit, reveal­ing that sev­er­al mutat­ed amino acid residues in the HR1 domain may be asso­ci­at­ed with enhanced inter­ac­tions with the HR2 domain. We pre­vi­ous­ly devel­oped a pan-coro­n­avirus fusion inhibitor, EK1, which tar­get­ed the HR1 domain and could inhib­it infec­tion by diver­gent human coro­n­avirus­es test­ed, includ­ing SARS-CoV and MERS-CoV. Here we gen­er­at­ed a series of lipopep­tides derived from EK1 and found that EK1C4 was the most potent fusion inhibitor against SARS-CoV­‑2 S pro­tein-medi­at­ed mem­brane fusion and pseudovirus infec­tion with IC50s of 1.3 and 15.8 nM, about 241- and 149-fold more potent than the orig­i­nal EK1 pep­tide, respec­tive­ly. EK1C4 was also high­ly effec­tive against mem­brane fusion and infec­tion of oth­er human coro­n­avirus pseudovirus­es test­ed, includ­ing SARS-CoV and MERS-CoV, as well as SARSr-CoVs, and potent­ly inhib­it­ed the repli­ca­tion of 5 live human coro­n­avirus­es exam­ined, includ­ing SARS-CoV­‑2. Intranasal appli­ca­tion of EK1C4 before or after chal­lenge with HCoV-OC43 pro­tect­ed mice from infec­tion, sug­gest­ing that EK1C4 could be used for pre­ven­tion and treat­ment of infec­tion by the cur­rent­ly cir­cu­lat­ing SARS-CoV­‑2 and oth­er emerg­ing SARSr-CoVs.

    A drug that might be effec­tive against not just ARS-CoV­‑2 but future emerg­ing “SARSr-CovSs” (bat coro­n­avirue­ses). That’s what this team may have devel­oped, based on their pre­vi­ous research on the mech­a­nisms of how relat­ed coro­n­avirus­es infect cells dur­ing this mem­brane fusion step. In par­tic­u­lar, research on the orig­i­nal SARS-CoV appears to be par­tic­u­lar­ly impor­tant because SARS-CoV­‑2 and SAR-CoV have an 89.8% genet­ic sequence sim­i­lar­i­ty for the S‑protein S2 sub­units. And when we do that com­par­i­son we find that SARS-CoV-2’s abil­i­ty to bind to the ACE2 recep­tor is 10-to-20 times greater than SARS-CoV, although that ACE2 RBD is in the S1 sub­unit of the S‑protein. It’s in the S2 sub­unit of the S‑protein where, where SARS-CoV and SARS-CoV­‑2 are 89.8% sim­i­lar, that we find the 6‑HB bun­dle of helices form after the find­ing of the S1 sub­unit to ACE2. That 6‑HB bun­dle is what fus­es with the tar­get cell mem­brane. And here we find sev­er­al amino acid muta­tions in SARS-CoV-2’s 6‑HB bun­dles that appear to enhance the for­ma­tion and sta­bil­i­ty of the bun­dle result­ing in what they described as a “much high­er capac­i­ty of mem­brane fusion than SARS-CoV”. So SARS-CoV­‑2 had the kinds of muta­tions in its genet­ic sequence that result­ed in actu­al changes in its pro­tein amino acid sequences and those amino acid muta­tions appear to have made SARS-CoV­‑2 much bet­ter at fus­ing with human cells than the orig­i­nal SARS-CoV virus:

    ...
    Coro­n­avirus­es (CoVs), the largest RNA virus­es iden­ti­fied so far, belong­ing to the Coro­n­aviri­dae fam­i­ly, are divid­ed into 4 gen­era, a‑, ß‑, d- and γ‑coronaviruses, while the ß‑coronaviruses are fur­ther divid­ed into A, B, C, and D lin­eages. The sev­en CoVs that can infect humans (HCoVs) include HCoV-229E and HCoV-NL63 in the a‑coronaviruses, HCoV-OC43 and HCoV-HKU1 in the ß‑coronaviruses lin­eage A, SARS-CoV and SARS-CoV­‑2 in the ß‑coronaviruses lin­eage B (ß‑B coro­n­avirus­es), and MERS-CoV in the ß‑coronaviruses lin­eage C.6 To devel­op spe­cif­ic SARS-CoV­‑2 fusion inhibitors, it is essen­tial to study the fusion capac­i­ty of SARS-CoV­‑2 com­pared to that of SARS-CoV. Par­tic­u­lar­ly, SARS-CoV and SARS-CoV­‑2 have 89.8% sequence iden­ti­ty in their spike (S) pro­teins S2 sub­units, which medi­ate the mem­brane fusion process, and both of their S1 sub­units uti­lize human angiotensin-con­vert­ing enzyme 2 (hACE2) as the recep­tor to infect human cells.6 Most impor­tant­ly, the ACE2-bind­ing affin­i­ty of the recep­tor-bind­ing domain (RBD) in S1 sub­unit of S pro­tein of SARS-CoV­‑2 is 10- to 20-fold high­er than that of SARS-CoV,Most impor­tant­ly, the ACE2-bind­ing affin­i­ty of the recep­tor-bind­ing domain (RBD) in S1 sub­unit of S pro­tein of SARS-CoV­‑2 is 10- to 20-fold high­er than that of SARS-CoV,12 which may con­tribute to the high­er infec­tiv­i­ty and trans­mis­si­bil­i­ty of SARS-CoV­‑2 com­pared to SARS-CoV. How­ev­er, it is unclear whether SARS-CoV­‑2 can medi­ate mem­brane fusion in a man­ner that exceeds the capac­i­ty of SARS-CoV.

    After bind­ing of RBD in S1 sub­unit of S pro­tein on the viri­on to the ACE2 recep­tor on the tar­get cell, the hep­tad repeat 1 (HR1) and 2 (HR2) domains in its S2 sub­unit of S pro­tein inter­act with each oth­er to form a six-helix bun­dle (6‑HB) fusion core, bring­ing viral and cel­lu­lar mem­branes into close prox­im­i­ty for fusion and infec­tion.13 There­fore, the 6‑HB fusion core struc­ture of SARS-CoV­‑2 and SARS-CoV S pro­teins should also be com­pared in order to inves­ti­gate the struc­tur­al basis for mem­brane fusion medi­at­ed by their S pro­teins and thus set the stage for the ratio­nal design of coro­n­avirus fusion inhibitors.

    ...

    In this study, we have shown that SARS-CoV­‑2 exhibits much high­er capac­i­ty of mem­brane fusion than SARS-CoV, sug­gest­ing that the fusion machin­ery of SARS-CoV­‑2 is an impor­tant tar­get for devel­op­ment of coro­n­avirus fusion inhibitors. We have solved the X‑ray crys­tal struc­ture of SARS-CoV‑2’s 6‑HB core and iden­ti­fied sev­er­al mutat­ed amino acid residues in HR1 domain respon­si­ble for its enhanced inter­ac­tions with HR2 domain. By con­ju­gat­ing the cho­les­terol mol­e­cule to the EK1 pep­tide, we found that one of the lipopep­tides, EK1C4, exhib­it­ed high­ly potent inhibito­ry activ­i­ty against SARS-CoV­‑2 S‑mediated mem­brane fusion and PsV infec­tion, about 240- and 150-fold more potent than EK1 pep­tide, respec­tive­ly. EK1C4 is also high­ly effec­tive against in vit­ro and in vivo infec­tion of some live HCoVs, such as SARS-CoV­‑2, HCoV-OC43 and MERS-CoV, sug­gest­ing poten­tial for fur­ther devel­op­ment as pan-CoV fusion inhibitor-based ther­a­peu­tics and pro­phy­lac­tics for treat­ment and pre­ven­tion of infec­tion by the cur­rent­ly cir­cu­lat­ing SARS-CoV­‑2 and MERS-CoV, as well as future reemerg­ing SARS-CoV and emerg­ing SARSr-CoVs.
    ...

    So that’s one of exam­ple of this virus hav­ing a remark­able abil­i­ty to inter­act with human cells not found in its clos­est viral cousins. It would be inter­est­ing to know if the muta­tions found in the SARS-CoV-2’s 6‑HB helix bun­dle were also found MERS since MERS also appears to have a sim­i­lar capac­i­ty to infect T cells. In oth­er words, are we see­ing a fea­ture found else­where show­ing up in this new virus or is this a total­ly new fea­ture?
    But at least it sounds like they do have some very potent can­di­date drug that might not only work on SARS-CoV­‑2 to treat cur­rent COVID-19 vic­tims but future coro­n­avirus­es too. Let’s hope this drug does­n’t end up hav­ing too many side effects. And, of course, let’s also hope knowl­edge of how this drug works does­n’t make it easy to design a drug-resis­tance ver­sion of the virus.

    Posted by Pterrafractyl | April 27, 2020, 3:37 pm
  13. @Pterrafractyl–

    Excel­lent work!

    We can but won­der, though, how much of this was engi­neered?

    Again, these virus­es were the focal point of some very pow­er­ful, capa­ble, and well-fund­ed inter­ests:

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

    And note oth­er “bio-occur­rences” that have hap­pened to Chi­na in the recent past:

    https://www.globalresearch.ca/china-coronavirus-shocking-update/5705196

    ” . . . . Just for infor­ma­tion

    In the past two years (dur­ing the trade war) Chi­na has suf­fered sev­er­al pan­demics:

    Feb­ru­ary 15, 2018: H7N4 bird flu. Sick­ened at least 1,600 peo­ple in Chi­na and killed more than 600. Many chick­ens killed. Chi­na needs to pur­chase US poul­try prod­ucts.
    June, 2018: H7N9 bird flu. Many chick­ens killed. Chi­na needs to pur­chase US poul­try prod­ucts.
    August, 2018: out­break of African swine flu. Same strain as Rus­sia, from Geor­gia. Mil­lions of pigs killed. Chi­na needs to pur­chase US pork prod­ucts.
    May 24, 2019: mas­sive infes­ta­tion of army­worms in 14 province-lev­el regions in Chi­na, which destroy most food crops. Quick­ly spread to more than 8,500 hectares of China’s grain pro­duc­tion. They pro­duce aston­ish­ing num­bers of eggs. Chi­na needs to pur­chase US agri­cul­tur­al prod­ucts – corn, soy­beans.
    Decem­ber, 2019: Coro­n­avirus appear­ance puts China’s econ­o­my on hold.
    Jan­u­ary, 2020:China is hit by a “high­ly path­o­gen­ic” strain of bird flu in Hunan province. Many chick­ens died, many oth­ers killed. Chi­na needs to pur­chase US poul­try prod­ucts.”

    Best,

    Dave

    Posted by Dave Emory | April 27, 2020, 4:56 pm

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