Thread by @RadCentrism

The Zoonoti Club released a pre-print: zenodo.org/record/5075888

Here's their TL;dr premise: Viruses that are "pre-adapted" to human ACE2 receptors would by definition stop mutating.

You don't need a virology background to know how silly this is from an evolutionary standpoint.

E.g.

"If SARS-CoV-2 resulted from attempts to adapt a SARSr-CoV for study in animal models, it would likely have acquired mutations like N501Y for efficient replication in that model"

LOL. Why would it "likely" have acquired these? They don't say.

"Recurring mutations...including N501Y...E484K/Q... similarly enhance viral infectivity and ACE2 binding, refuting claims that the SARS-CoV-2...was optimized for binding to human ACE2 upon...emergence"

Literal nonsense unless your premise is that viruses stop mutating.

Of course there's no mention of what Daszak/Shi were actually doing...by their own admission:

https://twitter.com/RadCentrism/status/1372971815081897987?s=20

"SARSCoV-2 is also notable for being a host generalist virus, capable of efficient transmission in multiple mammalian species...and large outbreaks have been documented in mink with spill-back to humans"

But its binding affinity is provably *HIGHEST* for humans...

"As for the vast majority of human viruses, the most parsimonious explanation for the origin of SARS-CoV-2 is a zoonotic event."

Prima facie false.

"The documented epidemiological history of the virus is comparable to previous animal market-associated outbreaks of coronaviruses with a simple route for human exposure."

Completely false. SARS1 emerged with sporadic infections, not optimized binding.

(From Baric himself: "Clinical data suggest that the sporadic early human SARS-CoV infections were significantly less pathogenic than later ones and that a progressive series of adaptive mutations was necessary for increased human-to-human transmission")
ncbi.nlm.nih.gov/pmc/articles/P…