I worked for many years in a lab, the accidental leak hypothesis was and still is what I consider the most probable. Calculate the joint probability of everything we know about the origin of SARS-CoV-2 happening and it should be obvious that the "lab leak" should be _thoroughly_ investigated before dismissing it.
p(Epidemic started in Wuhan) * p(origin in market right next to lab) * p(lab is one of 3 in the world to conduct gain-of-function research on conronaviruses) * p(lab scientists were notably sick prior to outbreak) * p(no accident ever happening in a lab) * p(et cetera) = very small number.
That's not evidence per se, but it does show you how probable a human error is.
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.
> 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.