I would like to see someone collect information about this hypothesis is a more organized fashion (not a youtube video), specifically to outline which labs are a possibility, who the people were at the labs, what their prior publications were, etc.
Also, for the other zoonosis, how did they arise? (I.e., in a city? In the country? etc.) Same question for other lab escapes.
This Nature article argues that two new features of SARS-CoV-2 look like they've undergone selection for humans or human-like hosts: the "receptor-binding motif (RBM) that directly contacts ACE2" and the "polybasic (furin) cleavage site". They argue that the virus had to acquire these features somewhere other than bats, and investigate several hypotheses:
1. Natural selection in an animal host before zoonotic transfer
2. Natural selection in humans following zoonotic transfer
3. Selection during passage
They think the third option is unlikely, though I don't entirely follow their argument:
"In theory, it is possible that SARS-CoV-2 acquired RBD mutations (Fig. 1a) during adaptation to passage in cell culture, as has been observed in studies of SARS-CoV11. The finding of SARS-CoV-like coronaviruses from pangolins with nearly identical RBDs, however, provides a much stronger and more parsimonious explanation of how SARS-CoV-2 acquired these via recombination or mutation19.
The acquisition of both the polybasic cleavage site and predicted O-linked glycans also argues against culture-based scenarios. New polybasic cleavage sites have been observed only after prolonged passage of low-pathogenicity avian influenza virus in vitro or in vivo17. Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of a progenitor virus with very high genetic similarity, which has not been described. Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described. Finally, the generation of the predicted O-linked glycans is also unlikely to have occurred due to cell-culture passage, as such features suggest the involvement of an immune system"
I think their argument boils down to "it's more parsimonious that SARS-CoV-2 ended up with RBD sites with ACE2 affinity via recombination with a pangolin virus than that it acquired it via selection in animal or cell culture, given the virus had not previously been described". I think this argument could be made cleaner, and that better steelman arguments for both "lab escape" and "zoonosis" origin could be produced.
Transmission via intermediary species is obviously possible. That the virus has 96% genetic structure to a known RatGN-13 virus in horseshoe bat i s not disputed. Neither is the real possiblity of SARS-Cov-2 originating in a natural gene swapping. What is not credible are the naive assertions of experts discounting a possible lab origin, by repeating essentially the "straw man" argument by K.G.Andersen, asserting that "synthetic lab origin" is impossible because of its proximity to known bat viruses. But no-one is arguing that. The... (read more)