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.
As an aside to anyone that isn't a professional scientist reading this thread: I'd just like to issue a caution that any time some supposed "expert" is telling you that you should listen to them because of their credentials, and not the merit of their argument, you should promptly ignore them. Extra points if they tell you that the argument is too complex for you to understand. If they can't explain it to a highschooler, they don't understand it either.
>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.
Actually, that's pretty much your entire argument. I'd rather not tie my HN identity to my real identity, as it's not unique to HN but all of my online life. All of my published work, with the exception of a single 1st author and a single 2nd author paper about CRISPR/Cas, is about viruses.
Here are some micrographs of viruses I work with that I took, today:
Feel free to reverse image search them or whatever. Edit: removed reference to specific lab for sake of anonymity.
>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)
Ah so now the goalposts have moved from "any virologist" to "people that use or study dangerous viruses in biosafety labs". Interesting.
>is that the virus likely came from a wild zoonotic crossover event.
I don't, and have never disputed that. You seem to think that the 3 points I laid out were some sort of thesis about the origins of the virus. They weren't and aren't. Just some interesting data that can be used to form a coherent hypothesis about the origins of the virus.
Similarly, none of the points in your "Reddit post of the year!" even remotely refute them. They cherry pick data.
Present an actual argument (here) and I'll engage on it based on the merits of the argument, not either of our credentials.
How is that true about anything I said regarding S/NS ratios, molecular clock analysis, the mosaic nature of the virus, the presence of O-linked glycans, the promiscuity and non-species specific nature of the spike protein, etc.
You conducted the mother of all handwaves and then asked me to present "actual" arguments. What? You never even approached the detail of any arguments I have made thus far.
I'm not going to make new ones until you provide some actual factual responses to the ones I've already made, thanks.
In case you don't want to find the link, here it is again: https://www.reddit.com/r/science/comments/gk6y95/covid19_did...
>I'm not going to make new ones until you provide some actual factual responses to the ones I've already made, thanks.
Considering I started the comment chain by offering a comment about biology, that you then derailed with some link to a reddit post that I fail to see how it applied, and then insinuated I'm not "a real virologist" (by the way great job just sidestepping my rebuttall to that) I'm a bit confused at this statement. If you're interested in the scientific discussion, you're welcome to have that discussion. So far all you've done is linked to a reddit post and listed some science terms, but failed to explain how any of that refutes my initial statement.
I'm kind of an idiot. Please, explain how CRISPR/Cas9 leaving off target mutation effects rules out that CoV 2 could have been genetically altered by humans in a lab. Please explain how having a bunch of Snps compared to its closest known neighbor somehow rules out that a 4 amino acid insertion was man made. Because I'm not making those connections, but then again, I'm apparently not a virologist.
I made statements. You claim to have refuted them (although 90% of your text has been questioning the credentials of others). I fail to see how you have refuted them. Maybe it's just over my head.
Edit: To get more specific:
2.1.1) You claim the virus is mosaic. True. What is not true is the conclusion you draw from that. Being mosaic does not mean that the virus isn't altered by humans. Take for instance, the furin site, which is a multiple-amino acid insertion, with a close match to, unless I'm mixing up stories, a pangolin. That hardly seems mosaic. So here's a scenario that explains that point away:
-The virus that was altered in the lab with GoF research is not derived exactly from the published RATG-13 genome. It is from a different isolate or extraction, and therefore contains a huge amount of SNPs and other mutations, something that RNA viruses can accomplish in extremely short amount of times (which we obviously both know). This could be the difference between sampling weeks apart.
And, the mosaicity (word?) of the virus does not adequately explain the furin site insertion.
2.2.1) Again, explains the mutations, not the insertion
2.2.2) Not sure what point you're making here, or how it applies to any of mine. Obviously it looks like a bat virus, probably because it is a bat virus. Still doesn't rule out the insertion of a furin site.
2.2.3) No one is suggesting that CRISPR-Cas9 was used to make the 1200 SNPs and other mutations across the genome. Obviously those could be natural, while the furin site insertion could have been done by people. Also, there are other ways to introduce mutations and insertions into RNA and DNA. Perhaps you've heard of PCR and infectious clones?
2.3) You're making a critical assumption that what was being tested and studied was a virus intended to hurt humans. (You also hilariously admit that it is the most effective it probably could be in the earlier sentence, but I'm not sure if you realize this). My hypothesis stated in my opening comment is not suggesting that.
I'm not suggesting someone took RATG-13, made 1200 SNPs and an insertion, all using CRISPR-Cas9, to design a virus to wipe out the human race.
Let me restate my hypothesis:
Someone was working in a lab, added a furin site to an ordinary coronavirus that didn't infect some type of organism, to see if it suddenly could. And guess what, it could. And oh no, it accidentally got out.
Nothing in your post refutes that in any way whatsoever. Your post is so far off in the weeds (suggesting that someone engineered 1200 SNPs into the virus, why on earth would they do that?) or that I am suggesting it was designed to be lethal to humans (I'm not) or that it's bad at being a virus because it's not lethal (which makes it a phenomenal virus) or that it's a terrible virus to study because the spike protein is promiscuous thanks to its furin site (which makes it good at jumping species which is a great reason to study that promiscuity).
Your argument flat out does not apply to my hypothesis, which is why I assume you have wasted most of your breath attacking the credentials of the people criticizing it.