1/ Here is a thread of the slides from my recent YouTube video on the evidence against a market origin of SARS-CoV-2. #COVID19#COVID#SARSCoV#OriginOfCovid
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18/ For all of my analyses of the origin of SARS-CoV-2 go to my website, DrQuay.com
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Here is my submitted testimony for the hearing today.
I approach the question of the origin with six 'Russian nesting dolls' of evidence, all supporting a lab-acquired infection.
14 sets of data document the outbreak began months before the market cases
8 observations from the market data not c/w a spillover.
A timeline of events at the WIV over six months c/w a lab reacting to a biosafety breech.
Data from a zoonosis with respect to animals, people, and viruses never seen with a spillover.
8 genome features c/w a synthetic virus. Probability one virus from nature has all of these features is one in 1.2 billion.
9 features described in the 2018 DEFUSE grant are found in SARS2.
The D614 unstable ancestor virus first seen in humans cannot passage in any animal without the D614G stabilization. Means the FCS was added last and infected a lab worker almost immediately and before animal passaging. Otherwise the first human cases would be D614G.
Next potential lab leak? The Nipah virus, 75% lethal,
Interesting how the envelope (A) and spike (E) genes of SARS-CoV-2 & RaTG13 but not the membrane or nucleocapsid genes segregate outside all bat CoVs with respect to codon usage?
This is behavior of a synthetic gene, constructed for improved laboratory amplification.
Every single bat CoV hates the CGG codon. Every. single. one.
Facts 1. CoV outbreak near CoV research institute (the John Stewart effect) of CoV found >1000 km to the south in nature but 96% match at WIV 2. No animal from market, city, province, or all of China with CoV. 80,000 tested 3. Single 'Virus Zero' with no posterior diversity
4. No pre-epidemic seroconversion. 9000+ tested 5. Spike Protein S1/S2 furin site never seen before in >1000 sarbecoviruses 6. CCG-CCG codon dimer never seen before in >1000 sarbecoviruses. 7. Recombination across subgenera to solve #5 & #6 either prohibited or rare.
8. RBD pre-adapted w best amino acid, 99.5%: Replacing every 1 of 200 amino acids of receptor binding region (3800 alternative AAs) leads to a poorer RBD.
9. WIV is only place in world combining 'gain-of-opportunity' CoV collection from nature and 'gain-of-function' research
For the non-scientist who might be confused by the CoV-2 origin debate, a proper sentence by a scientist has two parts. The first part is the data, the observation; the second part is the conclusion that follows from the data.
Based on testing 80,000 animals and finding no CoV-2 in any of them, one can conclude from statistics that the prevalence of CoV-2 where the testing was done must be less than 0.0004%.
Given that the zoonoses, SARS1 and MERS, had >85% positive tests in markets, the likelihood CoV-2 is a zoonosis like SARS1 or MERS is less than 1 in a 1,000,000.
I agree this is not an example of codon optimization for the same reason; it is done over a larger region.
But natural selection in betacoronaviruses has NEVER produced a -CGG-CGG- dimer codon pair. Repeating: there has never been this codon dimer in a coronavirus from nature.
So after scanning 580,000 betacoronavirus codons you suddenly have a -CGG-CGG- cannot be waved away with the 'sh#@' happens hypothesis. Remember, codons have a matching tRNA so putting the two rarest codons together is going to slow/stall transcription.
So we have a functional furin site that has never been seen in a betacoronavirus before that is coded for by a codon dimer that has never been seen before.