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FTR #1124 The Magic Virus Theory: The “Whole-of-Society Response”

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FTR #1124 This pro­gram was record­ed in one, 60-minute seg­ment. [6]    

[7]

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

Intro­duc­tion: This pro­gram takes stock of some of the remark­able fea­tures of the Covid-19 coro­n­avirus, to be seen in the con­text of a coun­try whose political/intellectual elites have accept­ed the “Mag­ic Bul­let The­o­ry.” (This is dis­cussed in–among oth­er pro­grams–The Guns of Novem­ber, Part [8] 2.)

It is our con­sid­ered opin­ion that the virus is part of the desta­bi­liza­tion effort against Chi­na and is found­ed upon research high­light­ed in, among oth­er pro­grams, FTR #‘s 1119 and [9] 1120.

As high­light­ed below, all of this must be eval­u­at­ed in light of the fact that the coor­di­na­tor of the anti-Chi­na effort–former Trump cam­paign man­ag­er Steve Ban­non–is a fas­cist. [10]

In addi­tion to review­ing how the Covid-19 virus infects human lung tis­sue and both the upper and low­er res­pi­ra­to­ry tracts, we note:

  1. The virus appears to have been [11] 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 abil­i­ty of this bat virus to infect ACE2 was present from day one. ” . . . . . The clos­est wild rel­a­tive of SARS-CoV­‑2 is found in bats [12], which sug­gests it orig­i­nat­ed in a bat, then jumped to humans either direct­ly or through anoth­er species. . . . 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 [13]of the Uni­ver­si­ty of Mary­land School of Med­i­cine. . . .
  3. Indeed, why was this “sev­enth virus” the one to infect humans “. . . . This fam­i­ly, the coro­n­avirus­es, includes just six oth­er mem­bers that infect humans. . . . . Why was this sev­enth coro­n­avirus the one to go pan­dem­ic? Sud­den­ly, what we do know about coro­n­avirus­es becomes a mat­ter of inter­na­tion­al con­cern. . . .”
  4. 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-func­tion’ 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.’ . . .”
  5. As dis­cussed in oth­er programs–including FTR #‘s 1117 [14] and 1121 [15], the “cytokine storms” that over­whelm the immune sys­tem of some Covid-19 vic­tims are symp­to­matic of oth­er virus­es that have under­gone either “Gain-of-Func­tion” alter­ation and/or genet­ic recov­ery and recreation–HN1 Avian Flu, SARS, and the 1918 “Span­ish Flu” virus: ” . . . . 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.  . . . .”

[16]In addi­tion, an arti­cle in Sci­ence Direct [17] 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.” Note the use of the word “strik­ing­ly” in this oth­er­wise dry and pedan­tic aca­d­e­m­ic pre­sen­ta­tion. It is VERY sig­nif­i­cant and–we suspect–betokens aware­ness on the part of the authors that “we aren’t in Kansas, any­more, Toto!” “. . . . STRIKINGLY [caps are ours–D.E.], 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. . . .”

The arti­cle also notes that the virus dif­fers sig­nif­i­cant­ly from oth­er coro­n­avirus­es of its type. ” . . . . Based on its genome sequence, 2019-nCoV belongs to lin­eage b of Beta­coro­n­avirus (Fig. 1 [17]A), 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., 2017 [17]Mbikay et al., 1997 [17]). Before the emer­gence of the 2019-nCoV, this impor­tant fea­ture was not observed in the lin­eage b of beta­coro­n­avirus­es. . . .”

[18]

Horse­shoe Bat

The fea­tures of the virus not­ed above must be seen in the con­text of the DARPA research [19] into bat coro­n­avirus­es:

  1. ” . . . . the Pentagon’s Defense Advanced Research Project Agency (DARPA), began spend­ing mil­lions on such research in 2018 and some of those Pen­ta­gon-fund­ed stud­ies were con­duct­ed at known U.S. mil­i­tary bioweapons labs bor­der­ing Chi­na and result­ed in the dis­cov­ery of dozens of new coro­n­avirus strains as recent­ly as last April. Fur­ther­more, the ties of the Pentagon’s main biode­fense lab to a virol­o­gy insti­tute in Wuhan, Chi­na — where the cur­rent out­break is believed to have begun — have been unre­port­ed in Eng­lish lan­guage media thus far. . . . For instance, DARPA spent $10 mil­lion on one project [20] in 2018 ‘to unrav­el the com­plex caus­es of bat-borne virus­es that have recent­ly made the jump to humans, caus­ing con­cern among glob­al health offi­cials.’ Anoth­er research project backed by both DARPA and NIH [21] saw researchers at Col­orado State Uni­ver­si­ty exam­ine the coro­n­avirus that caus­es Mid­dle East Res­pi­ra­to­ry Syn­drome (MERS) in bats and camels ‘to under­stand the role of these hosts in trans­mit­ting dis­ease to humans.’  . . . For instance, one study con­duct­ed in South­ern Chi­na in 2018 [22] result­ed in the dis­cov­ery of 89 new ‘nov­el bat coro­n­avirus’ strains that use the same recep­tor as the coro­n­avirus known as Mid­dle East Res­pi­ra­to­ry Syn­drome (MERS). That study was joint­ly fund­ed by the Chi­nese government’s Min­istry of Sci­ence and Tech­nol­o­gy, USAID — an orga­ni­za­tion long alleged to be a front for U.S. intel­li­gence [23], and the U.S. Nation­al Insti­tute of Health — which has col­lab­o­rat­ed with both the CIA and the Pen­ta­gon [24]on infec­tious dis­ease and bioweapons research.. . . .”
  2. DARPA is doing this work, in part, at bio­log­i­cal research facil­i­ties ring­ing both Chi­na and Rus­sia. ” . . . .  One of those stud­ies [25] focused on ‘Bat-Borne Zoonot­ic Dis­ease Emer­gence in West­ern Asia’ and involved the Lugar Cen­ter in Geor­gia, iden­ti­fied by for­mer Geor­gian gov­ern­ment offi­cials [26]the Russ­ian gov­ern­ment [27]and inde­pen­dent, inves­tiga­tive jour­nal­ist Dilyana Gay­tandzhie­va [28] as a covert U.S. bioweapons lab. . . . Anoth­er U.S. gov­ern­ment-fund­ed study that dis­cov­ered still more new strains of ‘nov­el bat coro­n­avirus’ was pub­lished just last year. Titled ‘Dis­cov­ery and Char­ac­ter­i­za­tion of Nov­el Bat Coro­n­avirus Lin­eages from Kaza­khstan [29],’ focused on ‘the bat fau­na of cen­tral Asia, which link Chi­na to east­ern Europe’ and the nov­el bat coro­n­avirus lin­eages dis­cov­ered dur­ing the study were found to be ‘close­ly relat­ed to bat coro­n­avirus­es from Chi­na, France, Spain, and South Africa, sug­gest­ing that co-cir­cu­la­tion of coro­n­avirus­es is com­mon in mul­ti­ple bat species with over­lap­ping geo­graph­i­cal dis­tri­b­u­tions.’ In oth­er words, the coro­n­avirus­es dis­cov­ered in this study were iden­ti­fied in bat pop­u­la­tions that migrate between Chi­na and Kaza­khstan, among oth­er coun­tries, and is close­ly relat­ed to bat coro­n­avirus­es in sev­er­al coun­tries, includ­ing Chi­na. . . .”
[30]

U.S. Army Med­ical Research Insti­tute of Infec­tious Disease–located at Ft. Det­rick and closed by the CDC for safe­ty vio­la­tions in August, 2019.

The unusu­al fea­tures of the virus must also be seen in the con­text of the Steve Ban­non-led anti-Chi­na desta­bi­liza­tion effort [31]. It is our opin­ion that the spread­ing of the virus is intend­ed to pro­voke the “Whole-of-soci­ety” response. As dis­cussed in FTR #947 [32], the dom­i­nant intel­lec­tu­al and polit­i­cal influ­ence on Ban­non is the Ital­ian fas­cist Julius Evola. Orig­i­nal­ly a sup­port­er of Mus­soli­ni, he ulti­mate­ly decid­ed Mus­soli­ni was too mod­er­ate and in an ide­o­log­i­cal “Gain-of-Func­tion” muta­tion, asso­ci­at­ed him­self with the Nazi SS, who were financ­ing his work by the end of World War II. 

Ban­non’s assess­ment of U.S.-China rela­tions amounts to a dec­la­ra­tion of “Totaler Krieg–Total War.” ” . . . ‘These are two sys­tems that are incom­pat­i­ble,’ Mr. Ban­non said of the Unit­ed States and Chi­na. ‘One side is going to win, and one side is going to lose.’ . . . .”

The coro­n­avirus attack we believe was unleashed on the U.S. and the world as a whole (to alien­ate it from Chi­na) and Chi­na itself (to inflect eco­nom­ic dam­age and stir up domes­tic unrest) is the man­i­fes­ta­tion of what the head of the FBI expressed: ” . . . . ‘I think it’s going to take a whole-of-soci­ety response by us.’ . . .”

Of para­mount impor­tance is the fact that state­ments being issued to the effect that the virus was not made in a lab­o­ra­to­ry are not just irrel­e­vant, but absurd. ANY virus can be made in a lab­o­ra­to­ry, from scratch, as is being done for the SARS-CoV­‑2 (Covid-19) virus.

The bro­mides being issued–all too predictably–that the virus could not have been/wasn’t made in a lab­o­ra­to­ry are the viro­log­i­cal equiv­a­lent of the Mag­ic Bul­let The­o­ry.

We first dis­cussed “Design­er Genes” in FTR #282 [33].

Ralph Baric–who did the gain-of-func­tion mod­i­fi­ca­tion on the Horse­shoe Bat coro­n­avirus, has been select­ed to engi­neer the Covid-19 [34].

” . . . . The remark­able abil­i­ty to ‘boot up’  virus­es from genet­ic instruc­tions is made pos­si­ble by com­pa­nies that man­u­fac­ture cus­tom DNA mol­e­cules, such as Inte­grat­ed DNA Tech­nol­o­gy, Twist Bio­science, and Atum. By order­ing the right genes, which cost a few thou­sand dol­lars, and then stitch­ing them togeth­er to cre­ate a copy of the coro­n­avirus genome, it’s pos­si­ble to inject the genet­ic mate­r­i­al into cells and jump-start the virus to life. The abil­i­ty to make a lethal virus from mail-order DNA was first demon­strat­ed 20 years ago. . . .”

Note what might be termed a “viro­log­ic Juras­sic Park” man­i­fes­ta­tion: ” . . . . The tech­nol­o­gy imme­di­ate­ly cre­at­ed bio-weapon wor­ries. . . . Researchers at the US Cen­ters for Dis­ease Con­trol and Pre­ven­tion (CDC) drove that point home in 2005 when they res­ur­rect­ed the influen­za virus [35] that killed tens of mil­lions in 1918–1919. . . .

A key fac­tor spurring our sus­pi­cion con­cern­ing genet­ic-engi­neer­ing of one or more vari­ant of the Covid-19 virus con­cerns a 2015 Gain-of-Func­tion exper­i­ment done by the above Ralph Bar­ic [34]: “Ralph Bar­ic, an infec­tious-dis­ease researcher at the Uni­ver­si­ty of North Car­oli­na at Chapel Hill, last week (Novem­ber 9) pub­lished a study on his team’s efforts to engi­neer a virus with the sur­face pro­tein of the SHC014 coro­n­avirus, found in horse­shoe bats in Chi­na, and the back­bone of one that caus­es human-like severe acute res­pi­ra­to­ry syn­drome (SARS) in mice. The hybrid virus could infect human air­way cells and caused dis­ease in mice. . . . The results demon­strate the abil­i­ty of the SHC014 sur­face pro­tein to bind and infect human cells, val­i­dat­ing con­cerns that this virus—or oth­er coro­n­avirus­es found in bat species—may be capa­ble of mak­ing the leap to peo­ple with­out first evolv­ing in an inter­me­di­ate host, Nature [36] report­ed. They also reignite a debate about whether that infor­ma­tion jus­ti­fies the risk of such work [37], known as gain-of-func­tion research. ‘If the [new] virus escaped, nobody could pre­dict the tra­jec­to­ry,’ Simon Wain-Hob­son, a virol­o­gist at the Pas­teur Insti­tute in Paris, told Nature. . . .”

Exem­pli­fy­ing the “See-No-Evil, Hear-No-Evil, Speak-No-Evil” myopia of the Main­stream Media, a New York Times [38] arti­cle blends edi­to­ri­al­iza­tion with stud­ied igno­rance: . . . . While con­spir­a­cy the­o­ries might false­ly claim the virus was con­coct­ed in a lab, the virus’s genome makes clear that it arose in bats [39]. There are many kinds of coro­n­avirus­es, which infect both humans and ani­mals. Dr. Boni and his col­leagues found that the genome of the new virus con­tains a num­ber of muta­tions in com­mon with strains of coro­n­avirus­es that infect bats. The most close­ly relat­ed coro­n­avirus is in a Chi­nese horse­shoe bat, the researchers found. But the new virus has gained some unique muta­tions since split­ting off from that bat virus decades ago. Dr. Boni said that ances­tral virus prob­a­bly gave rise to a num­ber of strains that infect­ed horse­shoe bats, and per­haps some­times oth­er ani­mals. . . .”

With Dr. Bar­ic hav­ing genet­i­cal­ly manip­u­lat­ed a Chi­nese horse­shoe bat coro­n­avirus to infect human lung tis­sue, Carl Zimmer–the author of the Times article–cannot hon­est­ly make such a state­ment. ANY virus can be syn­the­sized FROM SCRATCH in a lab­o­ra­to­ry, as we have seen.

An arti­cle pub­lished after this pro­gram was record­ed high­lights the VERY unusu­al [40] aspects of Covid-19. ” . . . . ‘I’ve been study­ing virus­es since 1978,’ Dr. James Hil­dreth [41], Mehar­ry Med­ical Col­lege CEO and an infec­tious dis­ease expert based out of Nashville, told Yahoo Finance’s On the Move [42] this week (video above). ‘And I think it’s fair to say we’ve not encoun­tered a virus quite like this, just because of the broad range of tis­sue types in our body it infects.’ . . .”

1a. Steve Bannon–one of the lumi­nar­ies of the “Alt-Right,” and a for­mer key Trump aide is cen­tral­ly involved in the anti-Chi­na effort. 

Note Ban­non and com­pa­ny’s net­work­ing with the Falun Gong cult and “Chi­nese Mus­lim Free­dom Fighters”–read “Uighurs.’ The desta­bi­liza­tion of Chi­na is the con­text in which the Covid-19 epi­dem­ic must be eval­u­at­ed.

“A New Red Scare Is Reshap­ing Wash­ing­ton” by Ana Swan­son; [31]The New York Times [31]; 7/20/2019. [31]

In a ball­room across from the Capi­tol build­ing, an unlike­ly group of mil­i­tary hawks, pop­ulist cru­saders, Chi­nese Mus­lim free­dom fight­ers [Uighurs–D.E.] and fol­low­ers of the Falun Gong has been meet­ing to warn any­one who will lis­ten that Chi­na pos­es an exis­ten­tial threat to the Unit­ed States that will not end until the Com­mu­nist Par­ty is over­thrown.

If the warn­ings sound straight out of the Cold War, they are. The Com­mit­tee on the Present Dan­ger, a long-defunct group that cam­paigned against the dan­gers of the Sovi­et Union in the 1970s and 1980s, has recent­ly been revived with the help of Stephen K. Ban­non, the president’s for­mer chief strate­gist, to warn against the dan­gers of Chi­na.

Once dis­missed as xeno­phobes and fringe ele­ments, the group’s mem­bers are find­ing their views increas­ing­ly embraced in Pres­i­dent Trump’s Wash­ing­ton, where skep­ti­cism and mis­trust of Chi­na have tak­en hold. Fear of Chi­na has spread across the gov­ern­ment, from the White House to Con­gress to fed­er­al agen­cies, where Beijing’s rise is unques­tion­ing­ly viewed as an eco­nom­ic and nation­al secu­ri­ty threat and the defin­ing chal­lenge of the 21st cen­tu­ry.

“These are two sys­tems that are incom­pat­i­ble,” Mr. Ban­non said of the Unit­ed States and Chi­na. “One side is going to win, and one side is going to lose.” . . . .

. . . . Anti-Chi­na sen­ti­ment has spread quick­ly, with Repub­li­cans and Democ­rats, labor union lead­ers, Fox News hosts and oth­ers warn­ing that China’s efforts to build up its mil­i­tary and advanced indus­tries threat­en America’s glob­al lead­er­ship, and that the Unit­ed States should respond aggres­sive­ly. Skep­ti­cism has seeped into near­ly every aspect of China’s inter­ac­tion with the Unit­ed States, with offi­cials ques­tion­ing China’s pres­ence on Amer­i­can stock mar­kets, its con­struc­tion of Amer­i­can sub­way cars and its pur­chase of social media net­works. . . .

. . . . At a Sen­ate hear­ing [43] last year, Christo­pher A. Wray, the F.B.I. direc­tor, said the Trump admin­is­tra­tion was try­ing to “view the Chi­na threat as not just a whole-of-gov­ern­ment threat, but a whole-of-soci­ety threat,” adding, “I think it’s going to take a whole-of-soci­ety response by us.” . . . .

1b. 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 [44] of DARPA research into bat-borne coro­n­avirus­es.

 “Why the Coro­n­avirus Has Been So Suc­cess­ful” Ed Yong; The Atlantic; 03/20/2020 [11]

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 [49] 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 symp­toms [50]spreads and kills more read­i­ly [51], 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 [52] 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 [53], 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 [12], 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 [13] 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 [54] 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 [55]. 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 [56] 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 [57], 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 [58], 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 [59] 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.

2a. In addi­tion, an arti­cle in Sci­ence Direct [17] 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. . . .”

“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. [17]

. . . . Based on its genome sequence, 2019-nCoV belongs to lin­eage b of Beta­coro­n­avirus (Fig. 1 [17]A), 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., 2017 [17]Mbikay et al., 1997 [17]). 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. 2 [17]Table 1 [17]), which were shown to be processed by furin exper­i­men­tal­ly (Le Coupanec et al., 2015 [17]Mille and Whit­tak­er, 2014 [17].

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. . . .

2b. Of para­mount impor­tance is the fact that the state­ments being issued that the virus was not made in a lab­o­ra­to­ry is not just irrel­e­vant, but absurd. ANY virus can be made in a lab­o­ra­to­ry, from scratch as is being done for the SARS-CoV­‑2 (Covid-19) virus.

The bro­mides being issued–all too predictably–that the virus could not have been/wasn’t made in a lab­o­ra­to­ry are the viro­log­i­cal equiv­a­lent of the Mag­ic Bul­let The­o­ry.

Ralph Baric–who did the gain-of-func­tion mod­i­fi­ca­tion on the Horse­shoe Bat coro­n­avirus, has been select­ed to engi­neer the Covid-19.

Note what might be termed a “viro­log­ic Juras­sic Park” man­i­fes­ta­tion: ” . . . . The tech­nol­o­gy imme­di­ate­ly cre­at­ed bio-weapon wor­ries. . . . Researchers at the US Cen­ters for Dis­ease Con­trol and Pre­ven­tion (CDC) drove that point home in 2005 when they res­ur­rect­ed the influen­za virus [35] that killed tens of mil­lions in 1918–1919. . . .

“Biol­o­gists rush to re-cre­ate the Chi­na coro­n­avirus from its DNA code” by Anto­nio Regal­a­do; MIT Tech­nol­o­gy Review; 02/15/2020 [60]

The world is watch­ing with alarm as Chi­na strug­gles to con­tain a dan­ger­ous new virus, now being called SARS-CoV­‑2. It has quar­an­tined entire cities, and the US has put a blan­ket ban on trav­ellers who’ve been there. Health offi­cials are scram­bling to under­stand how the virus is trans­mit­ted and how to treat patients.

But in one Uni­ver­si­ty of North Car­oli­na lab, there’s a dif­fer­ent race. Researchers are try­ing to cre­ate a copy of the virus. From scratch.

Led by Ralph Bar­ic [61], an expert in coronaviruses—which get their name from the crown-shaped spike they use to enter human cells—the North Car­oli­na team expects to recre­ate the virus start­ing only from com­put­er read­outs of its genet­ic sequence post­ed online by Chi­nese labs last month.

The remark­able abil­i­ty to “boot up” virus­es from genet­ic instruc­tions is made pos­si­ble by com­pa­nies that man­u­fac­ture cus­tom DNA mol­e­cules, such as Inte­grat­ed DNA Tech­nol­o­gy, Twist Bio­science, and Atum. By order­ing the right genes, which cost a few thou­sand dol­lars, and then stitch­ing them togeth­er to cre­ate a copy of the coro­n­avirus genome, it’s pos­si­ble to inject the genet­ic mate­r­i­al into cells and jump-start the virus to life.

The abil­i­ty to make a lethal virus from mail-order DNA was first demon­strat­ed 20 years ago. It’s enough of a bioter­ror­ism con­cern that com­pa­nies care­ful­ly mon­i­tor who is order­ing which genes. . . . The tech­nol­o­gy imme­di­ate­ly cre­at­ed bio-weapon wor­ries. . . . Researchers at the US Cen­ters for Dis­ease Con­trol and Pre­ven­tion (CDC) drove that point home in 2005 when they res­ur­rect­ed the influen­za virus [35] that killed tens of mil­lions in 1918–1919. . . .

2c. A key fac­tor spurring our sus­pi­cion con­cern­ing genet­ic-engi­neer­ing of one or more vari­ant of the Covid-19 virus con­cerns a 2015 Gain-of-Func­tion exper­i­ment: “Ralph Bar­ic, an infec­tious-dis­ease researcher at the Uni­ver­si­ty of North Car­oli­na at Chapel Hill, last week (Novem­ber 9) pub­lished a study on his team’s efforts to engi­neer a virus with the sur­face pro­tein of the SHC014 coro­n­avirus, found in horse­shoe bats in Chi­na, and the back­bone of one that caus­es human-like severe acute res­pi­ra­to­ry syn­drome (SARS) in mice. The hybrid virus could infect human air­way cells and caused dis­ease in mice. . . . The results demon­strate the abil­i­ty of the SHC014 sur­face pro­tein to bind and infect human cells, val­i­dat­ing con­cerns that this virus—or oth­er coro­n­avirus­es found in bat species—may be capa­ble of mak­ing the leap to peo­ple with­out first evolv­ing in an inter­me­di­ate host, Nature [36] report­ed. They also reignite a debate about whether that infor­ma­tion jus­ti­fies the risk of such work [37], known as gain-of-func­tion research. ‘If the [new] virus escaped, nobody could pre­dict the tra­jec­to­ry,’ Simon Wain-Hob­son, a virol­o­gist at the Pas­teur Insti­tute in Paris, told Nature. . . .”

“Lab-Made Coro­n­avirus Trig­gers Debate” by Jef Akst; The Sci­en­tist; 11/16/2015 [34]

Ralph Bar­ic, an infec­tious-dis­ease researcher at the Uni­ver­si­ty of North Car­oli­na at Chapel Hill, last week (Novem­ber 9) pub­lished a study on his team’s efforts to engi­neer a virus with the sur­face pro­tein of the SHC014 coro­n­avirus, found in horse­shoe bats in Chi­na, and the back­bone of one that caus­es human-like severe acute res­pi­ra­to­ry syn­drome (SARS) in mice. The hybrid virus could infect human air­way cells and caused dis­ease in mice, accord­ing to the team’s results, which were pub­lished in Nature Med­i­cine [62].

The results demon­strate the abil­i­ty of the SHC014 sur­face pro­tein to bind and infect human cells, val­i­dat­ing con­cerns that this virus—or oth­er coro­n­avirus­es found in bat species—may be capa­ble of mak­ing the leap to peo­ple with­out first evolv­ing in an inter­me­di­ate host, Nature [36] report­ed. They also reignite a debate about whether that infor­ma­tion jus­ti­fies the risk of such work [37], known as gain-of-func­tion research. “If the [new] virus escaped, nobody could pre­dict the tra­jec­to­ry,” Simon Wain-Hob­son, a virol­o­gist at the Pas­teur Insti­tute in Paris, told Nature. . . .

3. Whit­ney Webb has pro­vid­ed us with trou­bling insight into Pen­ta­gon research–some of which remains clas­si­fied:

“Bats, Gene Edit­ing and Bioweapons: Rec­cent DARPA Exper­i­ments Raise Con­cerns Amid Coro­n­avirus Out­break” by Whit­ney Webb; The Last Amer­i­can Vagabond; 1/30/2020. [63]

4. An arti­cle pub­lished after this pro­gram was record­ed high­lights the VERY unusu­al [40] aspects of Covid-19. ” . . . . ‘I’ve been study­ing virus­es since 1978,’ Dr. James Hil­dreth [41], Mehar­ry Med­ical Col­lege CEO and an infec­tious dis­ease expert based out of Nashville, told Yahoo Finance’s On the Move [42] this week (video above). ‘And I think it’s fair to say we’ve not encoun­tered a virus quite like this, just because of the broad range of tis­sue types in our body it infects.’ . . .”

“Coro­na Virus Expert: ‘We’ve Not Encoun­tered a Virus Quite Like This’” by Adri­ana Bel­monte [Yahoo Finance]; Yahoo News; 4/30/2020. [40]

The coro­n­avirus pan­dem­ic [64] has upend­ed nor­mal life across the world. 

There are over 1 mil­lion cas­es of COVID-19 [65] in the U.S., which is the glob­al leader in case count. World­wide, there are over 3 mil­lion cas­es. And for many doc­tors, the coro­n­avirus and its impacts are like noth­ing they’ve ever seen before.

“I’ve been study­ing virus­es since 1978,” Dr. James Hil­dreth [41], Mehar­ry Med­ical Col­lege CEO and an infec­tious dis­ease expert based out of Nashville, told Yahoo Finance’s On the Move [42] this week (video above). “And I think it’s fair to say we’ve not encoun­tered a virus quite like this, just because of the broad range of tis­sue types in our body it infects.”

The coro­n­avirus cre­ates the infec­tion known as COVID-19. The virus spreads through viral droplets from a cough or sneeze, which can trav­el into some­one else’s mouth, nose, or eyes. From there, accord­ing to Web­MD [66], it trav­els through the nasal pas­sage to the mucous mem­branes in your throat and latch­es on. 

With­in two to 14 days, a per­son can start show­ing symp­toms, which include fever, cough, chills, fatigue, and short­ness of breath. As the virus moves through the res­pi­ra­to­ry tract, it can inflame the lungs, caus­ing breath­ing dif­fi­cul­ties and lead­ing to pneu­mo­nia. 

“So any­one who has a com­pro­mised immune sys­tem, or their lungs are com­pro­mised in any way, they’re going to have real­ly poor out­comes,” Hil­dreth explained. 

The CDC has stat­ed [67] that those over the age of 65 and those with under­ly­ing health con­di­tions are most at risk for severe ill­ness from COVID-19. 

The peo­ple with under­ly­ing health con­di­tions at risk can be of any age. Those with asth­ma, chron­ic lung dis­ease, heart con­di­tions, obe­si­ty, dia­betes, liv­er dis­ease, kid­ney dis­ease, and those who are oth­er­wise immuno­com­pro­mised are espe­cial­ly vul­ner­a­ble. 

“It shuts down kid­neys,” Hil­dreth said. “As you’ve heard, it’s start­ing to cause blood clots in young peo­ple in their 30s and 40s who are dying of strokes. It caus­es real­ly severe lung dis­ease. And it also trig­gers some­thing called a cytokine storm [68], in which the immune sys­tem gets over exu­ber­ant and begins to destroy not just the virus, but the tis­sues around the virus.” 

Blood clot­ting is a new­er com­pli­ca­tion [69] that doc­tors have noticed in COVID-19 patients. A 41-year-old Broad­way actor named Nick Cordero, who has been in a med­ical­ly-induced coma for over a month because of the virus, had his leg ampu­tat­ed after devel­op­ing a clot. 

“We do need to find some­thing that can slow the virus down until we have a vac­cine,” Hil­dreth said. “But it’s fair to say that of all the virus­es that I’m aware that I’ve stud­ied or been involved with, this one is very dif­fer­ent, just in terms of the huge range of things that it does to the body.”

“It real­ly is an extra­or­di­nary chal­lenge, and like none we’ve seen before,” he added. “But I’m real­ly heart­ened by the fact that sci­en­tists all over the world have focused their atten­tion on it. And so, I’m con­fi­dent that we’re going to find some solu­tions in the com­ing months.”