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.
How do you suggest we would be able to completely engineer, from scratch, a novel virus with 1200 mutations spaced randomly throughout the genome, that would rescue properly and be capable of infecting a novel host? I know of no such modeling technology to accomplish this. All of these are phenomena that happen easily and constantly in a massive natural reservoir of any viral population.
And if you think it was not strictly "engineered" but instead "evolved" selectively by hand, then how can you escape the S/NS ratio problem? How can you escape the adaptation and glycosylation problem I describe in my original post? How could you avoid the issue of adapting to the host it was evolved in, and acquiring these "lab animal" or "cell culture" specific adaptation mutants that would then need to be somehow removed. Or it likely would not infect humans with any great reproductive efficiency. And then it would have an S protein that would be a bit more adapted to humans, as it has become over the course of the last year. As it's evolving in us, it is becoming better at infecting us. If it had been evolved in humans prior to the pandemic, this would not be as necessary and it would not happen on the scale it's currently happening.
And when exactly would China have started this little "experiment?" Where? With what subjects? How did they keep it secret?