And let's not even begin to think what will happen if there were to be evidence that this was an intentional release.
If Covid turns out to be a lab escape (which is a big if), the nation or lab it happened in is just the proximate cause. Deeper responsibility would lie with the institutions and individuals that pushed it despite the risks. No one knows the answer to this (edit: I mean to whether covid escaped from a lab), but it's an open question that deserves credible investigation. Having the investigator be one of the principal funders of the research being investigated is such...bad optics, to put it nicely, that one wonders how anyone thought that would be ok.
[1] https://mbio.asm.org/content/3/5/e00360-12
[2] https://www.nytimes.com/2012/01/08/opinion/sunday/an-enginee...
It seems like we don't have evidence, but the natural evolutionary experiment that's occurred provides a staggering amount. We can see from the virus phylogeny that:
1. The virus entered the human population in October 2019. All known SARS2 sequences are related in a single clade that, under very soft assumptions about mutation rate, would coalesce in late fall 2019. The first sequences we got, in early 2020, had only a handful of mutations between them. Nothing has ever arisen outside of this clade.
2. The virus entered humans with it's spike protein already fully adapted to the human ACE receptor protein. We can see this because there was not an accelerated evolution in this protein. We did not see changes in the viral genome resulting in a significant phenotypic change until the b.1.1.7 and other "third wave" variants arose. This stands in intense contrast to every other zoonotic transfer we know of. Adaptation always occurs because biology is different enough that different viral configurations provide immediate gain, and through continuous mutation the virus is exploring a huge space of these all the time. The fact that it doesn't mutate rapidly indicates it is near a strong local optimum.
One way of understanding the significance of this is by thinking of the virus as a learned model which is learning a solution to the problem of its own survival. What this evidence shows is that is appeared already optimized. We see this because over an incredible number of update steps (many quadrillions perhaps, with each human infection being like a minibatch, and each viral replication like a step) there was no significant reduction in test loss (viral survival). We randomly picked a perfect initial model. Either that first virus was lucky in a way that is similar to guessing a perfect solution, which has a probability so low as to be fanciful, or it had already in incorporated all the readily-usa le information about the human ACE receptor.
Do we have evidence? What is the probability of this pattern occuring in the case of a natural spillover? It's 1:atoms-in-the universe level. Finding a virus already so optimized to humans by randomly sampling from existing ones is like the kind of collision probability level that we comfortably use to build cryptocurrency castles that assume key non-collision. In the case of a virus optimized by serial passage in the lab? Frankly it's indistinguishable from that.
This is untrue. I'd point to this quote:
“It’s pretty apparent that there’s this evolutionary arms race between the receptor binding domain and ACE2 that’s happening within the bats themselves,” says Tyler Starr, a postdoc in the lab of genome scientist Jesse Bloom at Fred Hutchinson Cancer Research Center. “Whatever it’s doing is ratcheting up this evolution and sometimes spitting out things that can bind potentially to many different ACE2s, including ours.”[1]
The unique thing about COVID is the transmission and the long incubation time.
There are plenty of naturally occurring mutations that have occurred that are more contagious than COVID (AIDS R0=~4.5, Ebola=~2.5 are two major ones that spring to mind). And SARS1 had a very similar binding behaviour, and the jumping behavior via civets is very similar to COVID.
[1] https://cen.acs.org/biological-chemistry/infectious-disease/...
This is a good summary of the current consensus:
It is clear from our analysis that viruses closely related to SARS-CoV-2 have been circulating in horseshoe bats for many decades. The unsampled diversity descended from the SARS-CoV-2/RaTG13 common ancestor forms a clade of bat sarbecoviruses with generalist properties—with respect to their ability to infect a range of mammalian cells—that facilitated its jump to humans and may do so again. Although the human ACE2-compatible RBD was very likely to have been present in a bat sarbecovirus lineage that ultimately led to SARS-CoV-2, this RBD sequence has hitherto been found in only a few pangolin viruses. Furthermore, the other key feature thought to be instrumental in the ability of SARS-CoV-2 to infect humans—a polybasic cleavage site insertion in the S protein—has not yet been seen in another close bat relative of the SARS-CoV-2 virus.