While viruses do mutate a lot, if the sequence were that labile, then you would expect there to be a lot of divergence around the furin cleavage site. We don't really see that, so the site is stable. So, is there something special about that DNA sequence (including the synonymous wobble pairs) that make this a random walk gradient descent minimum? Or is the mutation rate lower than you think.

All I'm saying is when people say "this mutation is super rare therefore it MUST have been manmade!", I'm skeptical. Even the most stable DNA sequences have mutations occasionally, because mutations happen for a bunch of totally uncorrelated reasons. It could have been manmade, but it could have also been made by a stray cosmic ray. To say a particular sequence "proves" that the virus is manmade is...sketchy at best.

Nobody is claiming proof. Don't move the goalposts.

This article is....suggestive, to say the least. So I'm at least responding to the article.

This article is worse than useless because it places a pseudoscientific veneer around something (to make it sound plausible) while still being almost certainly wrong.

Only gatekeepers would want to keep scientific evidence from commoners, instead of teaching them that said evidence isn't anywhere close to proof yet.

every major university in the us contains physical copies of all the published articles (IE, people who wanted to learn more, but couldn't afford to subscribe to every journal), annd the rest are on arxiv. Nobody is gatekeeping the evidence.

The reality is that average people simply aren't qualified to deal with the subtlety and complexity of ambiguous data, and the adversaries of public health can just make a video that lies and convince millions of people with seductive, but wrong, ideas. It's extremely rare to have a society which is scientifically savvy enough to understand these sorts of things.

What evidence?

The mutation rate for proofreading ssRNA viruses is, affair, about 10^-7 per nt per replication. If we don’t see a particular variant nt it is (from the top of my head) because it didn’t “survive” the drift events or that there is strong positive selection on the sequence.

(Preemptive) Synonymous mutations are able to be selected, as they affect speed of translation and protein folding due to stalled ribosomes.