zlacker

I've read a few articles, skimmed a few papers and sent them to friends. The counterargument is that there still aren't enough similarities.

The mutations on covid 19 are Really Different compared to the known and studied viruses. If it was a lab leak of an engineered chimera, you'd be able to see that A proteins came from virus X and B proteins came from virus Y and Z, but that hasn't been shown to be the case. From what I understand there are a bunch of smaller mutations across a lot of proteins resulting in something that doesn't really line up with known and studied genomes.

This paper actually goes through and compares the DNA of covid 19 against several other studied viruses: https://www.nature.com/articles/s41579-020-00459-7

>>Jarwai+(OP)
Of course that says little about SARS-CoV-2 relative to all the other viruses we don't know about, either sitting in a Chinese government lab, or in a bat cave somewhere.

I guess I don't find the argument "we can't figure out how to reconstruct SARS-COV-2 from known viruses" very convincing on either side.

>>teorem+5a
That's fair. I wouldn't say that it's "we can't figure it out" but rather that "doing so takes a lot of mutations and thus resources that may be difficult to do under the table"

Sitting in a cave somewhere implies not being studied, right? Which is more the "natural mutation" thing.

Sitting in some government lab is a different story and depends on belief in scientific institutions to do science and publish peer reviewed papers and all that jazz.

>>Jarwai+9b
Another question is how you can make a virus evolve in the direction you want. 20 years of bat evolution would not necessarily bring a furin cleavage site, so how do you make sure it does?

>>Jarwai+(OP)
My understanding is that this is what gain of function research is all about. Accelerated evolution within a lab towards infecting a specific species.

It doesn't have to be crispr introducing reach mutation.

>>Husafa+7P
RaTG13 is decades of evolution away from SARS-CoV-2, all over its genome.

You don't get there by splicing an ACE2 spike onto an RaTG13 backbone and passing it through a dozen mice. That gives you something that still looks similar to RaTG13 and infects mice.

The ACE2 spike also looks most similar to a previously unknown ACE2-binding spike protein found in malaysian pangolins.

So WIV would have had to have discovered that pangolin spike-protein, kept it secret, spliced it into an RaTG13 backbone, then not used mice but passed it through a species like that had a human-like ACE2 for a decade and millions of animals.

An alternative hypothesis is that Charles Darwin did that experiment.