Some things (going by memory here) that seem to support the hypothesis:
1) Major point of differentiation for this virus is that compared to it's closest known relatives, it has acquired a furin site (eukaryotic protein cleavage site) that enhances its virulence.
2) That furin site RNA contains a non-canonical amino acid codon
3) That non-canonical codon contains a restriction site that could easily be used to track, whether, say, your added furin site is surviving multiple cell passages, by performing a restriction digest and running the fragments on a cell.
Like I said above, it's circumstantial, but this is all very normal. Both adding the furin site (how does coronavirus evolve into something more virulent?) and tracking it that way. Then all it takes is someone to get infected (EVERYONE working in biology has broken at least one lab safety rule in their life, even in BSL4) and either not be symptomatic and realize, or not say anything.
I describe the evidence in detail in this detailed longform post I wrote on reddit a few months back: Hi, I have a PhD in virology focused on emerging viruses, and a few months back I wrote a very lengthy and involved piece full of sources.
And in there, I describe exactly how wrong your point 1 is. And how misguided your point 3 is.
The post also won a "best of r/science 2020" award!
You can find it here: https://www.reddit.com/r/science/comments/gk6y95/covid19_did...
See under "Addendum to Q2"
As a virologist, who "engineers viruses", I also take some offense to this line: >The virus itself, to the eye of any virologist, is clearly not engineered.
I also suspect that the viruses referenced in the featured article would object to that line as well.
Petrovsky, for instance, if you look at his google scholar, hasn't published a paper in a virology journal in the 10 years that I looked. He's published in some predatory journals, ones I wouldn't be caught dead publishing in.
He's also gotten /close/, I guess, by publishing about tuberculosis. But it really is different and the man clearly has never done any viral biosafety work or worked or supervised work in any secure facilities working with viruses.
If he did, I think he might be more cautious about being so cavalier with the probabilities here.
David Relman studies the gut microbiome.
I have no reason to believe you're a virologist with any training other than your word, but that isn't actually all that important to my argument.
Using viruses in your research doesn't make you a virologist any more than using pens in an art school thesis makes you an expert in ballpoint pens.
All of that aside, the consensus among people who actually use or study dangerous viruses in biosafety labs (both those for and against gain of function research, btw) is that the virus likely came from a wild zoonotic crossover event.
Not a malicious lab leak.