This isn't a smoking gun, but it's big. Thread summary:
SARS-CoV2 has a short genetic sequence (furin site) that makes it ultra-infectious in humans and allows it infect many tissue types and jump between species. No closely related (beta CoV) virus has ever been found with one
SARS-CoV2 has a short genetic sequence (furin site) that makes it ultra-infectious in humans and allows it infect many tissue types and jump between species. No closely related (beta CoV) virus has ever been found with one
In 2006 a virology lab reported experimental insertion of a furin site that produced a big jump in the ability of the altered virus to infect human cells. There insert was at precisely the same location in the genome as the furin site in SARS-CoV2.
Others have found natural insertions at this location in beta CoVs, but never a furin site. Why? Given the effect of modifications at this location, selection 'experiments' and 'discovers' useful changes. But furin is like a cheat-code for transmission--Hard to find, and powerful
Upshot: We've been assured that if a lab wanted to make a highly infectious SARS-CoV, they'd never have produced this SARS-CoV2 because they'd have predicted such a virus would fail. That's false. If one wanted to study SARS-CoV in human tissue this change would have been logical
*If* the Covid-19 pandemic is due to an experimentally furin-enhanced SARS-CoV, *then* many of the most troubling aspects (e.g. range of symptoms, high transmisability) of the disease are the result of Gain of Function research, not natural properties of known wild SARS-CoVs.
Corrections, amendments, challenges are welcome.
I explore the question with @ydeigin on the DarkHorse Podcast
