6 ms·

....I presented a lot of extremely detailed arguments backed up by references in my original post and you just dismissed them by saying they "cherry pick" data.

....I presented a lot of extremely detailed arguments backed up by references in my original post and you just dismissed them by saying they "cherry pick" data. 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_not_come_from_the_wuhan_institute_of/ https://www.reddit.com/r/science/comments/gk6y95/covid19_did...

COGlory 6y ago
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.
- jeduehr 6y ago
  You spend an awful lot of time attacking me and not very much time attacking my arguments. That's not very scientific of you. I said I had no way to know you were actually a virologist, which I didn't. It isn't really important to the discussion though, as I said. Can we talk about this like adults? Thanks. I'm only gonna address the science in your post from here on out. I want to make it clear I never insulted you or attacked your character, I only said I had no way to know you were a virologist and only could go off of your word. I get your hypothesis now that you have fully stated it. And here are some questions that need answers. Where did they get the virus? It's not anything like any coronavirus we know of before SARS-CoV-2 emerged in humans, it's 1200 away from RATG-13. What experimental question were they trying to answer? We already know that the furin cleavage site is necessary for some aspects of pathogenicity, but not the ones canonically thought important (cell entry for SARS-1 for example, since furin doesn't actually cleave SARS-1 or MERS). Why would they test a random unrelated coronavirus' site? Why not try the SARS-CoV-1 site? Or the MERS site? Why was it a furin site in the first place? And why did they do it on the weirdly promiscuous SARS-2 ACE2 and not in a virus like RATG-13? Re: cleavage site, I go into extreme detail about how possible it is for cleavage sites to evolve in nature here and here: -https://www.reddit.com/r/science/comments/gk6y95/covid19_did_not_come_from_the_wuhan_institute_of/fqpbys1/ https://www.reddit.com/r/science/comments/gk6y95/covid19_did... -https://news.ycombinator.com/item?id=26757881 https://news.ycombinator.com/item?id=26757881 It's really not that unusual for a cleavage site to evolve in nature, and especially not when we consider that furin cleavage sites are mutagenicity islands. It absolutely could have evolved from recombination with a distantly related coronavirus that has an extremely similar site. Also, the cleavage site isn't even that long. Short stretches of nucleotides like that, upwards of 15-30 nucleotides, can absolutely evolve over the course of 50-70 years. Happens literally all the time. In influenza it happens on much shorter time scales. I provide evidence to that effect in the above posts. Yes I actually address the idea of using recombinatorial cloning to make SARS-CoV-2 at several points in my post. Nothing about the furin cleavage site makes it more likely to be unnatural than it is natural? And so far, I don't see any compelling reason to believe that anyone would take a completely undiscovered and undescribed virus out of nature, not describe it or publish on it at all, and then start inserting random furin sites into it from random other coronaviruses. Why would they be doing that? Is it technically /possible/? Yes, but I see no reason why it is more likely than a natural emergence.

COGlory 6y ago

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.

jeduehr 6y ago
You spend an awful lot of time attacking me and not very much time attacking my arguments. That's not very scientific of you. I said I had no way to know you were actually a virologist, which I didn't. It isn't really important to the discussion though, as I said. Can we talk about this like adults? Thanks. I'm only gonna address the science in your post from here on out. I want to make it clear I never insulted you or attacked your character, I only said I had no way to know you were a virologist and only could go off of your word. I get your hypothesis now that you have fully stated it. And here are some questions that need answers. Where did they get the virus? It's not anything like any coronavirus we know of before SARS-CoV-2 emerged in humans, it's 1200 away from RATG-13. What experimental question were they trying to answer? We already know that the furin cleavage site is necessary for some aspects of pathogenicity, but not the ones canonically thought important (cell entry for SARS-1 for example, since furin doesn't actually cleave SARS-1 or MERS). Why would they test a random unrelated coronavirus' site? Why not try the SARS-CoV-1 site? Or the MERS site? Why was it a furin site in the first place? And why did they do it on the weirdly promiscuous SARS-2 ACE2 and not in a virus like RATG-13? Re: cleavage site, I go into extreme detail about how possible it is for cleavage sites to evolve in nature here and here: -https://www.reddit.com/r/science/comments/gk6y95/covid19_did_not_come_from_the_wuhan_institute_of/fqpbys1/ https://www.reddit.com/r/science/comments/gk6y95/covid19_did... -https://news.ycombinator.com/item?id=26757881 https://news.ycombinator.com/item?id=26757881 It's really not that unusual for a cleavage site to evolve in nature, and especially not when we consider that furin cleavage sites are mutagenicity islands. It absolutely could have evolved from recombination with a distantly related coronavirus that has an extremely similar site. Also, the cleavage site isn't even that long. Short stretches of nucleotides like that, upwards of 15-30 nucleotides, can absolutely evolve over the course of 50-70 years. Happens literally all the time. In influenza it happens on much shorter time scales. I provide evidence to that effect in the above posts. Yes I actually address the idea of using recombinatorial cloning to make SARS-CoV-2 at several points in my post. Nothing about the furin cleavage site makes it more likely to be unnatural than it is natural? And so far, I don't see any compelling reason to believe that anyone would take a completely undiscovered and undescribed virus out of nature, not describe it or publish on it at all, and then start inserting random furin sites into it from random other coronaviruses. Why would they be doing that? Is it technically /possible/? Yes, but I see no reason why it is more likely than a natural emergence.