Your arguments are not arranged in any sort of logical way against the hypothesis I discussed which set this whole chain off. I examined the one that you claimed refuted it, and failed to see how it applied. If you apply it to my statement, we could actually discuss it, but until you do that I'm lost by what you're supposedly proving with it.
>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.