[542458]

I can’t help but feel you’re taking all the “for” factors and none of the “against”, then bending the “for” factors even further.

Calling the market “right next to the lab” is a bit of a stretch - it’s a three and a half hour walk.

The scientists getting sick early doesn’t actually seem to be confirmed - there’s still debate in the US intelligence community whether it’s true. And going to the hospital because you’re sick means something a bit different in China where primary care is rare.

And as for “against”... no mention of the virus not matching any backbones in use for genetic experimentation, or the suboptimal binding to humans, both of which would suggest against engineering.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7095063/

[tpfour]

Let me make this clear: I don't know for certain what happened. But after updating my priors, I believe it's highly probable that the outbreak came from human error.

Also, I never once mentioned engineering. There's a lab 280m away from the market that has one of the largest bat virus samples in the world.

I would have no problem revising my priors, but for the moment I still consider the lab leak human error hypothesis still the most reasonable explanation.

[tripletao]

Every published backbone used for genetic experimentation was at some point unpublished. The WIV had the biggest program in the world to sample novel SARS-like coronaviruses from nature, plus the ability to engineer them in the lab. In the words of David Relman:

> This argument [that SARS-CoV-2 must be natural since it doesn't use a known backbone] fails to acknowledge the possibility that two or more as yet undisclosed ancestors (i.e., more proximal ancestors than RaTG13 and RmYN02) had already been discovered and were being studied in a laboratory—for example, one with the SARS-CoV-2 backbone and spike protein receptor-binding domain, and the other with the SARS-CoV-2 polybasic furin cleavage site. It would have been a logical next step to wonder about the properties of a recombinant virus and then create it in the laboratory.

https://www.pnas.org/content/117/47/29246

Note also that the WIV's public database of viral genomes went offline in Sept 2019, and hasn't come back.

As to the binding, Andersen looked at the binding of SARS-CoV-2's RBD to human ACE2 in silico, and found that it was suboptimal. But that proves only that the RBD wasn't designed in silico using his software workflow. Among unnatural origins, it's far more likely that the RBD either evolved naturally (as Relman proposed above) in a different virus, or evolved quasi-naturally in the lab during culture in human cells or in humanized mice. Andersen's argument doesn't address these more likely possibilities.

[jkhdigital]

> no mention of the virus not matching any backbones in use for genetic experimentation, or the suboptimal binding to humans

Are you going to cite sources? And then are you going to cite the other sources which have addressed both of these weak counter arguments? Some of us have done a lot of homework on this one, so you need to bring your A game.

[henearkr]

The optimal binding for humans would have been SARS-COV1 at that time, so the fact it was not reused shows the suboptimality.

[tpfour]

There is a vast amount of unpublished research, not because of malicious intentions, but because it's either still ongoing, or abandoned, or postponed, or waiting for other results, or for review, or qualified specialists to help, whatever.

The VF article specifically mentions that the closest known virus was 96% similar (vs 90% for SARS-CoV-1), and had actually been renamed by the scientists studying it and that fact hadn't been put forward to the community.

It can still be shown that this has a completely natural (i.e. no human error involved) origin, but the burden of proof gets higher every day. It's much more probable that human error is involved, which is something that happens every day.

[henearkr]

General closeness does not guarantee that the binding site was as much efficient.

The SARS-CoV-1 had a spike protein binding very efficiently to humans, but that was not the case for the other, hence the above said suboptimality.