5 ms·

But there are about 1200 mutations! From the source [0] Dr. Deurh's references: > there are 931 synonymous substitutions and 145 missense substitutions between

But there are about 1200 mutations! From the source [0] Dr. Deurh's references: > there are 931 synonymous substitutions and 145 missense substitutions between SARS-CoV-2 and RaTG13. The other ORF regions (90%) are identical between SARS-CoV-2 and RaTG13 Nobody does 931 + 145 substitutions for function of gain, do they? Dr Duehr says "this many differences or mutations (the mosaic) in the virus, can only reasonably have been made in nature." There was another section of his post that talked about how the receptor was optimized to work with multiple species (bat, pangolin, etc), something it would do evolving in nature. Now I'm not going to insist that there are never lab leaks. In fact, reading one article on this subject, I was shocked by how many lab leaks there are, every year, even right here in the U.S. [1]: > Young pointed to documents she recently obtained through the Freedom of Information Act, which revealed that laboratories in the United States "reported more than 450 accidents during 2015 through 2019 while experimenting with some of the world's most dangerous pathogens." > Such pathogens, Young revealed, included anthrax, Ebola, plague, and more. > "In nearly all reported cases, regulators deemed the breaches serious enough to put workers at risk of becoming infected," she wrote. "As a result, more than 660 U.S. scientists and other lab workers involved in the incidents underwent medical assessment or treatment with preventative medications." Based on Dr. Deuhr's thoroughly documented post I just don't think that covid-19 was a lab leak. Some viruses jump between animals and humans, this looks like it was just another one. I would rather that we talk about all the other lab leaks that go on. Who's making the decisions to put the public at risk? Is there anything we can do about any of this? There was a flu in the mid-1970s due to a lab leak. It's only a matter of time until something else happens. [0] https://www.futuremedicine.com/doi/full/10.2217/fvl-2020-0066 https://www.futuremedicine.com/doi/full/10.2217/fvl-2020-006... [1] https://www.theblaze.com/news/investigative-reporter-lab-leaks-wuhan-covid https://www.theblaze.com/news/investigative-reporter-lab-lea...

awb 5y ago
Not a virologist, but according to Root Claim the strongest evidence for a lab leak is: 1. Furin Cleavage > SARS-CoV-2 has a furin cleavage site - an amino acid sequence that causes the protease furin to cut the virus in a way that facilitates its entry into cells. This feature is missing in related coronaviruses, and its placement in the genetic code looks like an insertion rather than a mutation, making it less likely to develop in nature. 2. Adapted to humans from 1st known case > It appears that there was one index case of COVID-19, rather than multiple jumps from nature to humans, as was the case in many other pandemics. Additionally, SARS-CoV-2 was already well adapted for human infection from the first known cases. 3. Wuhan Lab > There is some weak evidence regarding lax security and procedures at the Wuhan Institute of Virology. > The WIV explicitly stated that they were not working on SARS-CoV-2 prior to the outbreak. > However, on December 30, when Dr. Shi Zheng-Li was informed of the COVID-19 outbreak, changes were made to her bat virus database, making it look like she was trying to dissociate her lab's research from the COVID-19 outbreak. > Then, in January 2020, WIV researchers published a paper claiming to have found a previously unknown coronavirus named RaTG13 that was a 96% match with SARS-CoV-2. > But RaTG13 is a new name given to BtCoV/4991, a coronavirus that the WIV discovered (along with many other viruses) when they examined a bat cave after six miners contracted a pneumonia-like disease and three died. This, and other anomalies surrounding WIV’s handling of RaTG13, are indicative of attempts to minimize WIV involvement. BTW, if you think they’re wrong, you can contact them here and win a potential $100k: https://www.rootclaim.com/think_rootclaim_is_wrong https://www.rootclaim.com/think_rootclaim_is_wrong
- mikem170 5y ago
  On the cleavage site, from [0]: > Second, what about the polybasic cleavage site and the o-linked glycan? We have seen, with other viruses, the ability to develop polybasic cleavage sites when put under just the right conditions for long periods of time. While unlikely, this piece of the virus could plausibly be developed through selection in a lab setting. However, what is near impossible is the development of the o-linked glycan addition motif. This is because the pressure to develop this glycan shield requires avoiding an intact immune system. This type of selection cannot occur using cell culture, and there is no known animal model that would allow for selection of human-like ACE2 binding and avoidance of immune recognition. This strongly implies SARS-CoV-2 could not have been developed in a lab, even by a system of simulated natural selection This was a really informative source. I keep finding sources like this explaining that the genetics (the most trustable evidence) point to a natural evolution of this virus as the much more likely origin. Occam's razor. I personally don't have $100k to take rootclaim up on the challenge of proving them wrong. I appreciate their presentation, which is much more thorough than other sources, but I don't think they are giving fair weight to contradictory genetic evidence and explanations (like the o-linked glycan mentioned above, which seems to invalidate their point on the cleavage site being made in a lab). For their genetic-based points (cleavage and adaptation) they admit a chance of being wrong in both cases, that nature could have done this. But this is probably what happened, there are hundreds of coronaviruses and hundreds of animals that can host them [1]. [0] https://leelabvirus.host/covid19/origins-part3 https://leelabvirus.host/covid19/origins-part3 [1] https://bigthink.com/coronavirus/coronavirus-animals https://bigthink.com/coronavirus/coronavirus-animals
  - awb 5y ago
    Thanks, this is an interesting debate. But like swine flu or avian flu wouldn’t we expect to see some animal populations impacted by COVID prior to it’s jump to humans?
  - salawat 5y ago
    Relevant excerpts: >So what’s the best hypothesis? The available data suggests a two-step process that may have given rise to SARS-CoV-2: A bat coronavirus likely infected an intermediary animal (potentially a Malayan pangolin) where it recombined with a non-bat coronavirus. Over time, either in the intermediary animal or while in humans, SARS-CoV-2 developed additional mutations: a polybasic cleavage site and a nearby o-linked glycan addition site. It’s worth noting there are actually two competing hypotheses. In hypothesis 1, SARS-CoV-2 gains its new tools before spillover into humans. In hypothesis 2, SARS-CoV-2 gains these tools while amplifying in humans. If hypothesis 2 is correct, then when SARS-CoV-2 first infected humans, it probably replicated and spread less well (like MERS, another human coronavirus). Over multiple replication cycles, the virus made mistakes and some mutants gained the advantage and began spreading efficiently among humans. If this is true, then we can implement better measures to monitor humans for new infections, and catch spillover viruses before they “get good” at spreading in humans. Most scientists will look at the data gathered so far and say we’re on the right track because: All the current data fits our hypotheses Our hypotheses are the most parsimonious and best satisfy Occam’s Razor Our hypotheses are testable and falsifiable This strongly implies the virus was not designed or modified in a lab A follow up section digs into two methods of man-made virus engineering. The article addresses each individually and concludes neither in isolation fits the bill. It does not address both in combination. Which is a glaring omission given that both methodologies being well defined mean that they can be applied in a staged manner trivially, and in fact, doing so would be, to me, the most practicable way to innovate. Apply every tool I know in discrete steps to leverage the best aspects of both methods. Then there is this section: >Second, what about the polybasic cleavage site and the o-linked glycan? We have seen, with other viruses, the ability to develop polybasic cleavage sites when put under just the right conditions for long periods of time. While unlikely, this piece of the virus could plausibly be developed through selection in a lab setting. However, what is near impossible is the development of the o-linked glycan addition motif. This is because the pressure to develop this glycan shield requires avoiding an intact immune system. This type of selection cannot occur using cell culture, and there is no known animal model that would allow for selection of human-like ACE2 binding and avoidance of immune recognition. This strongly implies SARS-CoV-2 could not have been developed in a lab, even by a system of simulated natural selection. Which did not touch on whether O-linked glycan formation is a trait exclusive to human immune systems and not present in bats or pangolins, which are both jawed mammals in possesion of adaptive immune systems, capable of applying said pressure as far as I am aware. This may be blatantly obvious to a zoologist, or immunologist, but the answer to such a question is not at all obvious to me. If there is someone with said knowledge or who knows someone with it, it would be much obliged for a sharing thereof. Especially given that the chemical reaction is not exactly uncommon apparently. https://en.m.wikipedia.org/wiki/O-linked_glycosylation https://en.m.wikipedia.org/wiki/O-linked_glycosylation

awb 5y ago

Not a virologist, but according to Root Claim the strongest evidence for a lab leak is: 1. Furin Cleavage > SARS-CoV-2 has a furin cleavage site - an amino acid sequence that causes the protease furin to cut the virus in a way that facilitates its entry into cells. This feature is missing in related coronaviruses, and its placement in the genetic code looks like an insertion rather than a mutation, making it less likely to develop in nature. 2. Adapted to humans from 1st known case > It appears that there was one index case of COVID-19, rather than multiple jumps from nature to humans, as was the case in many other pandemics. Additionally, SARS-CoV-2 was already well adapted for human infection from the first known cases. 3. Wuhan Lab > There is some weak evidence regarding lax security and procedures at the Wuhan Institute of Virology. > The WIV explicitly stated that they were not working on SARS-CoV-2 prior to the outbreak. > However, on December 30, when Dr. Shi Zheng-Li was informed of the COVID-19 outbreak, changes were made to her bat virus database, making it look like she was trying to dissociate her lab's research from the COVID-19 outbreak. > Then, in January 2020, WIV researchers published a paper claiming to have found a previously unknown coronavirus named RaTG13 that was a 96% match with SARS-CoV-2. > But RaTG13 is a new name given to BtCoV/4991, a coronavirus that the WIV discovered (along with many other viruses) when they examined a bat cave after six miners contracted a pneumonia-like disease and three died. This, and other anomalies surrounding WIV’s handling of RaTG13, are indicative of attempts to minimize WIV involvement. BTW, if you think they’re wrong, you can contact them here and win a potential $100k: https://www.rootclaim.com/think_rootclaim_is_wrong https://www.rootclaim.com/think_rootclaim_is_wrong

mikem170 5y ago
On the cleavage site, from [0]: > Second, what about the polybasic cleavage site and the o-linked glycan? We have seen, with other viruses, the ability to develop polybasic cleavage sites when put under just the right conditions for long periods of time. While unlikely, this piece of the virus could plausibly be developed through selection in a lab setting. However, what is near impossible is the development of the o-linked glycan addition motif. This is because the pressure to develop this glycan shield requires avoiding an intact immune system. This type of selection cannot occur using cell culture, and there is no known animal model that would allow for selection of human-like ACE2 binding and avoidance of immune recognition. This strongly implies SARS-CoV-2 could not have been developed in a lab, even by a system of simulated natural selection This was a really informative source. I keep finding sources like this explaining that the genetics (the most trustable evidence) point to a natural evolution of this virus as the much more likely origin. Occam's razor. I personally don't have $100k to take rootclaim up on the challenge of proving them wrong. I appreciate their presentation, which is much more thorough than other sources, but I don't think they are giving fair weight to contradictory genetic evidence and explanations (like the o-linked glycan mentioned above, which seems to invalidate their point on the cleavage site being made in a lab). For their genetic-based points (cleavage and adaptation) they admit a chance of being wrong in both cases, that nature could have done this. But this is probably what happened, there are hundreds of coronaviruses and hundreds of animals that can host them [1]. [0] https://leelabvirus.host/covid19/origins-part3 https://leelabvirus.host/covid19/origins-part3 [1] https://bigthink.com/coronavirus/coronavirus-animals https://bigthink.com/coronavirus/coronavirus-animals
- awb 5y ago
  Thanks, this is an interesting debate. But like swine flu or avian flu wouldn’t we expect to see some animal populations impacted by COVID prior to it’s jump to humans?
- salawat 5y ago
  Relevant excerpts: >So what’s the best hypothesis? The available data suggests a two-step process that may have given rise to SARS-CoV-2: A bat coronavirus likely infected an intermediary animal (potentially a Malayan pangolin) where it recombined with a non-bat coronavirus. Over time, either in the intermediary animal or while in humans, SARS-CoV-2 developed additional mutations: a polybasic cleavage site and a nearby o-linked glycan addition site. It’s worth noting there are actually two competing hypotheses. In hypothesis 1, SARS-CoV-2 gains its new tools before spillover into humans. In hypothesis 2, SARS-CoV-2 gains these tools while amplifying in humans. If hypothesis 2 is correct, then when SARS-CoV-2 first infected humans, it probably replicated and spread less well (like MERS, another human coronavirus). Over multiple replication cycles, the virus made mistakes and some mutants gained the advantage and began spreading efficiently among humans. If this is true, then we can implement better measures to monitor humans for new infections, and catch spillover viruses before they “get good” at spreading in humans. Most scientists will look at the data gathered so far and say we’re on the right track because: All the current data fits our hypotheses Our hypotheses are the most parsimonious and best satisfy Occam’s Razor Our hypotheses are testable and falsifiable This strongly implies the virus was not designed or modified in a lab A follow up section digs into two methods of man-made virus engineering. The article addresses each individually and concludes neither in isolation fits the bill. It does not address both in combination. Which is a glaring omission given that both methodologies being well defined mean that they can be applied in a staged manner trivially, and in fact, doing so would be, to me, the most practicable way to innovate. Apply every tool I know in discrete steps to leverage the best aspects of both methods. Then there is this section: >Second, what about the polybasic cleavage site and the o-linked glycan? We have seen, with other viruses, the ability to develop polybasic cleavage sites when put under just the right conditions for long periods of time. While unlikely, this piece of the virus could plausibly be developed through selection in a lab setting. However, what is near impossible is the development of the o-linked glycan addition motif. This is because the pressure to develop this glycan shield requires avoiding an intact immune system. This type of selection cannot occur using cell culture, and there is no known animal model that would allow for selection of human-like ACE2 binding and avoidance of immune recognition. This strongly implies SARS-CoV-2 could not have been developed in a lab, even by a system of simulated natural selection. Which did not touch on whether O-linked glycan formation is a trait exclusive to human immune systems and not present in bats or pangolins, which are both jawed mammals in possesion of adaptive immune systems, capable of applying said pressure as far as I am aware. This may be blatantly obvious to a zoologist, or immunologist, but the answer to such a question is not at all obvious to me. If there is someone with said knowledge or who knows someone with it, it would be much obliged for a sharing thereof. Especially given that the chemical reaction is not exactly uncommon apparently. https://en.m.wikipedia.org/wiki/O-linked_glycosylation https://en.m.wikipedia.org/wiki/O-linked_glycosylation