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Thread: The Potential Lab Origin of COVID-19

  1. #21
    Ludicus's Avatar Comes Limitis
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    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by sumskilz View Post
    There is a certain amount of intuition involved.. circumstantial evidence .....I would also add this suspicious order...
    I don't know or care about what Pompeo said.
    But you should,ask him to make proof of what he says, end of the story.
    Mike Pompeo: 'enormous evidence' coronavirus came from ...


    Peter Daszak, the one man who has the most to lose if it turns SARS-CoV-2 was actually leaked from the WIV lab.
    More insinuations.

    And again, I insist- once again-in a joint open letter to the U.S. National Institutes for Health (NIH) last Thursday, 77 American Nobel laureates in science expressed their deep concern...The letter... came one day after 31 science societies criticized cancellation, saying it politicized science.

    This is what is at stake. Not "intuitions,suspicions and the Deszak who has the most to lose."And 77 nobel prizes and 31 science societies.All of them sold their souls to China, so it seems.

    The pandemic of conspiracy theories is bad for democracy and bad for our mental health.

    Divide et Impera. With the elections just around the corner, the fire of hate must be kept burning: normality is undesirable.
    W.B.Yats writes in the "The Second Coming" (1921) : "Things fall apart; the center cannot hold". The poem is more actual than ever: the "rough beast" of the next age feeds itself from mysticism, aversion to democracy and science.
    Last edited by Ludicus; June 09, 2020 at 09:08 AM.
    Il y a quelque chose de pire que d'avoir une âme perverse. C’est d'avoir une âme habituée
    Charles Péguy

    Every human society must justify its inequalities: reasons must be found because, without them, the whole political and social edifice is in danger of collapsing”.
    Thomas Piketty

  2. #22

    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by Ludicus View Post
    And again, I insist- once again-in a joint open letter to the U.S. National Institutes for Health (NIH) last Thursday, 77 American Nobel laureates in science expressed their deep concern...The letter... came one day after 31 science societies criticized cancellation, saying it politicized science.
    I think it’s hyperbole. Daszak’s grant was $3.7 million. Only the $600,000 slated to go to the WIV was suspended pending an investigation, and some of it has already been spent. There is nothing that prevents him from continuing to collaborate with WIV, he just can’t use taxpayer dollars. The fastest way for him to free the rest of his grant would be to help facilitate an investigation, why wouldn’t he want to? Not that I think the Chinese government would agree to it, but then that would say something.

    The various noises being made by Pompeo are political, but there are valid concerns that aren't partisan. During the last few years of the Obama administration, Daszak wouldn’t have been able to use any public funds for gain of function research since there was a moratorium instituted in 2014 over safety concerns. It's hard to make a good assessment of whether or not gain of function research's benefits outweigh its risks if you don't know whether or not it was responsible for the biggest pandemic in generations.
    Last edited by sumskilz; June 09, 2020 at 10:08 AM.
    Quote Originally Posted by Enros View Post
    You don't seem to be familiar with how the burden of proof works in when discussing social justice. It's not like science where it lies on the one making the claim. If someone claims to be oppressed, they don't have to prove it.


  3. #23
    Ludicus's Avatar Comes Limitis
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    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by sumskilz View Post
    I think it’s hyperbole...It's hard to make a good assessment of whether or not gain of function research's benefits outweigh its risks if you don't know whether or not it was responsible for the biggest pandemic in generations.
    Common sense says that the claims of 77 Nobel prize mercenaries and 31 Chinese secret societies are not an hyperbole, the claims are meant to be taken literally.

    The letter from the scientific societies was organized by the American Society for Biochemistry and Molecular Biology. I quote,
    Our aim with this effort is to stand up for a scientific enterprise that should be free of political influence on sound scientific research.The continued politicization of science during this pandemic crisis is an alarming trend that is risking not only the integrity of science, but also the lives of citizens.
    --
    How the Right-Wing Disinformation Loop Helped
    This funding was pulled 10 days after Rep. Matt Gaetz, a Trump ally and Florida Republican, appeared on one of the president’s favorite Fox News programs and, without evidence, connected EcoHealth’s grant to China “birth[ing] a monster” virus. “The NIH gives this $3.7 million grant to the Wuhan Institute of Virology, they then advertise that they need coronavirus researchers. Following that, coronavirus erupts in Wuhan,” he told Tucker Carlson on April 14.
    Trump is the new Terminator,the isolationist is a threat to progress and international organizations. The center of the new "yellow peril" is the P4 Chinese laboratory...
    Il y a quelque chose de pire que d'avoir une âme perverse. C’est d'avoir une âme habituée
    Charles Péguy

    Every human society must justify its inequalities: reasons must be found because, without them, the whole political and social edifice is in danger of collapsing”.
    Thomas Piketty

  4. #24

    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by Ludicus View Post
    Common sense says that the claims of 77 Nobel prize mercenaries and 31 Chinese secret societies are not an hyperbole, the claims are meant to be taken literally.

    The letter from the scientific societies was organized by the American Society for Biochemistry and Molecular Biology. I quote,
    I have seen how the medical lie for politically correct reasons. Ans given China's enormous political and financial clout, I am sure they would use such influence, and even Nobel prize winners, worried about grant money, mifht not be immuned to such influence. AI wonder what these same Nobel lauriates stance on Tibet or the Chinese treatment of Uighurs and other dissedents.

    I remember how scientist said AIDS was not transfered by blood, depite obvious evidence otherwise*, only changing their stance when overwhelming evidence made that claim no longer supportable and when it was too late for many victims.. As a consequence, steps that might have been taken to were not, and famous people like the black tennis star Authur Ashe and the writer Isaac Asimov contracted HIV througj blood tranfusions. Nor were the standard reporting practices of sexually transmitted diseases like syphilis implemented. Hospital workers were fired foe wanting to wear safety protection when dealing with AIDS protection, the same protection that later became mandatory, but for dealing with all patients whether it was needed for them or not.

    *It was known for that HIV was in the blood, and that hemophiliacs represented a large 2nd largest group of AIDS victims after gay men. Clearly transfer by blood was a very likely possibility, yet scientist denied thst possibility, no doubt Nobel lauriates among them.



    However, ths Nobel lauriates are correct in that nothing in the evidence indicates that COVID-19 might not have been natural, and if unless there is positive proof COVID-19 was created in a lab, I agree it is unjustified and reckless to say it was.


    [URL="https://www.vanityfair.com/news/2020/05/right-wing-media-trump-kill-coronavirus-research-funding"]How the Right-Wing Disinformation Loop Helped
    Ol, I understand why there were so many papers debunking the idea COVID-19 could come out of the lab and why they were so insistent about that. Still, I don't see their evidence proving absolutely COVID-19 is natural, only that it is the most probable possibility. It is a natural tendency to overstate a case when trying to combat false claims.






    Trump is the new Terminator,the isolationist is a threat to progress and international organizations. The center of the new "yellow peril" is the P4 Chinese laboratory...
    China is a threat, asserting all kinds of claims in the China Seas, and its lax safety standards pose a major health risk to the rest of the world, as COVID-19 demonstrates. Even if COVID-19 was natural, the disease ariseas a byproduct out of Chinese practices. The scandals I listed previously were just some of the scandals China was not able cover up, despite its influence, and China has used its influence to prevent recognition of Tawain, and stifle any criticism of its colonization of Tibet or handling of dissidents and ethnic minorities like thr Uighurs.

    So while China didn't deliberstely manufacture COVID-19, or deliberately spread it, it does not mean China isn't a serious threat in other ways. Just ask the Tibetans when there aren't Chinese around, one of the Uighur minorities.
    Last edited by Common Soldier; June 09, 2020 at 06:52 PM.

  5. #25

    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by Ludicus View Post
    Common sense says that the claims of 77 Nobel prize mercenaries and 31 Chinese secret societies are not an hyperbole, the claims are meant to be taken literally.

    The letter from the scientific societies was organized by the American Society for Biochemistry and Molecular Biology.
    I was referring to the media coverage. For example, the claim that EcoHealth "lost the ability to look for new viruses in China" is BS.

    As far as the letter itself, nobody wants to have their grant suspended mid-project. Although I don't have much sympathy for Daszak due to the lack of integrity in his media blitz. When he claims there is no evidence of gene editing therefore scientists know it couldn't have come from the Wuhan lab, that's not just a non sequitur, it's a lie of omission meant to confuse an audience without the foreknowledge to catch it.

    In contrast, Andersen et al concede that while the insertions could have come about while being passaged in a lab, they have reason to believe it more likely evolved in nature. I disagree based on a different assessment of the weight placed on various aspects of the circumstantial evidence, but theirs is an example of how one constructs an argument with scientific integrity. Daszak is in a position to be aware of unpublished evidence relevant to the matter, so his resorting to dishonest arguments is a red flag.

    Meanwhile, the Wuhan Institute of Virology themselves are taking the lab escape hypothesis more seriously. The abstract of their correspondence published two days ago reads as follows (note the last line I bolded):

    The unprecedented pandemic of pneumonia caused by a novel coronavirus, SARS-CoV-2, in China and beyond has had major public health impacts on a global scale [1, 2]. Although bats are regarded as the most likely natural hosts for SARS-CoV-2 [3], the origins of the virus remain unclear. Here, we report a novel bat-derived coronavirus, denoted RmYN02, identified from a metagenomic analysis of samples from 227 bats collected from Yunnan Province in China between May and October 2019. Notably, RmYN02 shares 93.3% nucleotide identity with SARS-CoV-2 at the scale of the complete virus genome and 97.2% identity in the 1ab gene, in which it is the closest relative of SARS-CoV-2 reported to date. In contrast, RmYN02 showed low sequence identity (61.3%) to SARS-CoV-2 in the receptor-binding domain (RBD) and might not bind to angiotensin-converting enzyme 2 (ACE2). Critically, and in a similar manner to SARS-CoV-2, RmYN02 was characterized by the insertion of multiple amino acids at the junction site of the S1 and S2 sub units of the spike (S) protein. This provides strong evidence that such insertion events can occur naturally in animal betacoronaviruses.
    Of course this is beside the point for the subject of this thread, since anything that can occur in nature can likewise occur during passage in human cell cultures, and would of course evolve much faster in the latter case. Nevertheless, I have to wonder why an extensive scientific argument needed to be made that it is possible that the furin cleavage site could have evolved naturally when we all know that to suggest otherwise is just a far fetched conspiracy theory.

    Counter Birger Sørensen, Ronen Shemesh, etc., I never really believed it was likely that the furin cleavage site insertion was the product of gene editing, nor do I now, but if Daszak and the WIV keep protesting too much, they might sway me. This study actually demonstrates that WIV had almost all the components in their lab to create SARS-CoV-2 as a chimera. Although it still wouldn't have been human adapted without passaging, but it is well-documented that they were passaging chimeric coronavirues in collaboration with Daszak's team.

    Quote Originally Posted by Ludicus View Post
    How the Right-Wing Disinformation Loop Helped

    Trump is the new Terminator,the isolationist is a threat to progress and international organizations. The center of the new "yellow peril" is the P4 Chinese laboratory...
    It's amusing to me that the people hysterical about Trump/Pompeo/Gaetz's inflated allegations haven't figured out that if the WIV escape hypothesis is true, they have a convoluted way to blame the entire global pandemic on Trump. Are they not clever enough or just too caught up in their own reflexive hysteria to be able to think straight? Keep harping on about conspiracy theories too long and they'll miss their chance.
    Quote Originally Posted by Enros View Post
    You don't seem to be familiar with how the burden of proof works in when discussing social justice. It's not like science where it lies on the one making the claim. If someone claims to be oppressed, they don't have to prove it.


  6. #26
    Ludicus's Avatar Comes Limitis
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    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by sumskilz View Post
    I have to wonder why an extensive scientific argument needed to be made that it is possible that the furin cleavage site could have evolved naturally when we all know that to suggest otherwise is just a far fetched conspiracy theory.
    An abstruse conclusion, a mistrust so intense it borders on political paranoia. This is a very enlightening article, btw.

    Our study reaffirms that bats, particularly those of the genus Rhinolophus, are important natural reservoirs for coronaviruses and currently harbor the closest relatives of SARS-CoV-2, although this picture may change with increased wildlife sampling. In this context it is striking that the RmYN02 virus identified here in Rhinolophus malayanus is the closest relative of SARS-CoV-2 in the long 1ab replicase gene, although the virus itself has a complex history of recombination. Finally, the observation that RmYN02 contains an insertion of multiple amino acids at the S1/S2 cleavage site in the spike protein clearly indicates that events of this kind are a natural and expected component of coronavirus evolution
    -----
    Sumskilz, it all boils down to this,
    Evidence of COVID's natural origin mounts even as conspiracy theorie about chinese lab refuses to die

    A survey taken of 6,300 Americans found 44 percent believe the coronavirus was probably created in a lab, while 56 percent said this is likely or definitely untrue. The belief was held by 50 percent of Republicans surveyed, compared with just 37 percent of Democrats.
    As The Washington Post reported: “Beijing has led an authoritarian crackdown on information about the initial coronavirus outbreak, while Washington has demonstrated a cavalier willingness to fuel theories about a Chinese lab accident without presenting any evidence.

    Caught in the middle are scientists from both countries, facing questions about their research and doubts about whether their years-long collaboration can continue amid escalating geopolitical tension.
    Quote Originally Posted by sumskilz View Post
    people hysterical about Trump... Are they not clever enough or just too caught up in their own reflexive hysteria to be able to think straight?
    Hysterical? nope. Trump, in his infinite stupidity, is beyond any meaningful adjective.Aren't the Trump's acolytes clever enough to be able to think straight?

    Nobody directly blames the pandemic on Trump, China-or anybody else. This isn't the first pandemic, and won't be the last one.Let's go back in time, 2003. SARS 3: are we ready? - NCBI,

    "This is about lack of imagination,” Ali Khan, formerly of the C.D.C., said. Read the New Yorker, Why Weren't We Ready for the Coronavirus? | The New Yorker

    The U.S. has fared worse than other countries not because it lacked information or funding but because it failed to learn the lessons of the last outbreaks...Shi and Daszak and their colleagues not only warned the world, three years ago, that a new sars-like disease was possible. They held up for inspection, as though with a pair of tongs, a close variant of the virus that would cause the covid-19 pandemic...Furthermore, they added, it wasn’t just one virus that we needed to be wary of, since various sars-like viruses capable of using the ace-2 receptor “are still circulating among bats in this region.”

    ....Dennis Carroll, a former research virologist, led a pandemic-threats unit at the U.S. Agency for International Development for almost fifteen years. In 2009, he created a large program called predict, dispersing about two hundred million dollars in grants to support discovery of potentially dangerous new viruses before they spill over into humans. That program is ending, due to “the ascension of risk averse bureaucrats,” he told the Times, last October. He mentioned the White House closure of the N.S.C. health directorate as a parallel instance, and said that both Congress and the Administrations of George W. Bush and Barack Obama were “enormously supportive,” but then came the current chill winds.

    ....The U.S. is not alone. “The global community has a really difficult time investing in what you think of as risk,” Carroll told me recently. Spending big money is itself a form of risk, especially if it’s public money, even if you’re spending it to insure against a greater risk. What if you spend a billion dollars, or ten billion—small change compared with what covid-19 is now costing—and the pandemic doesn’t occur during your term in office? “There’s very little appetite for that when the threat isn’t clear and present.

    ...When sars happens, when a swine-flu pandemic happens, when an Ebola epidemic happens, political leaders and private donors react with fretful largesse, but when the crisis ends, he said, “we see a total collapse of those kinds of investments.”
    ---
    Quote Originally Posted by Common Soldier View Post
    China is a threat
    We have already learned from "The Reliability On Reporting On Chinese History (TWCenter) that the Chinese culture has a higher tendency to lie, and the Chinese people is the most dishonest people.
    Coronavirus is another US-China battle behind the scenes...
    ----

    Edit,
    With that said ....The Risks of Building Too Many Bio Labs | The New Yorker
    Excerpts,
    ...The new coronavirus has plunged us into an infectious-disease crisis with which we are struggling to cope. As we respond, the years-long debate over N.B.A.F. raises worrying questions about American biodefense policy. Will more labs help us fight outbreaks? Or are we building too many labs in too many places? Who, if anyone, is responsible for making sure that labs are well-run—or for saying “stop”?

    In a 2015 report, “Biolabs in Your Backyard,” USA Today documented hundreds of safety violations and accidents at high-containment labs, and, in 2014, the Guardian found that British high-security labs had experienced more than a hundred near-misses or accidents in five years.

    In 2016, Lentzos and another biosecurity expert, Gregory Koblentz, of George Mason University, published a paper contending that a dramatic increase in the number of labs and scientists working on dangerous pathogens was adding to our collective risk. They identified a number of potential dangers, including accidental releases, worker infections, theft, and insider threats.
    Last edited by Ludicus; June 10, 2020 at 01:55 PM.
    Il y a quelque chose de pire que d'avoir une âme perverse. C’est d'avoir une âme habituée
    Charles Péguy

    Every human society must justify its inequalities: reasons must be found because, without them, the whole political and social edifice is in danger of collapsing”.
    Thomas Piketty

  7. #27
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    Default Re: The Potential Lab Origin of COVID-19

    Ludicus, what scientific arguments can you bring in regards to Covid-19s origin?
    Patronised by Pontifex Maximus
    Quote Originally Posted by Himster View Post
    The trick is to never be honest. That's what this social phenomenon is engineering: publicly conform, or else.

  8. #28

    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by Ludicus View Post
    An abstruse conclusion, a mistrust so intense it borders on political paranoia. This is a very enlightening article, btw.
    Based on the partial sentence you underlined, I don't think you understood it. RmYN02 is only closest to SARS-CoV-2 at the furin cleavage site insertion. It differs from SARS-CoV-2 by ~39% in the receptor-binding domain. It seems like you might be confusing RmYN02 with RaTG13. It's actually RaTG13 that is closest to SARS-CoV-2. RmYN02 and RaTG13 were sampled from two different species of bats. The receptor-binding domain looks like it came from pangolins.

    So in their data, we see that SARS-CoV-2 is almost identical to RaTG13, except that it has a receptor-binding domain like a Pangolin coronavirus (the part that enables it to infect humans) and the spike protein very similar to that of RmYN02 (the part that enables it to be so virulent in humans). All of which were present in the Wuhan lab. This actually strengthens the case of those who are arguing that gene editing was involved, because SARS-CoV-2 looks like a RaTG13 backbone with the receptor-binding domain from pangolin/MP789/2019 and a spike protein from RmYN02. It would be quite a coincidence if the only two parts RaTG13 (or a closely related virus) acquired from other coronaviruses just happened to be those that make it so dangerous to people. In fact, that implies deliberate gain of function manipulation. Nevertheless, the spike protein in this hypothesized chimera would have had to have undergone further selection, such as during passages through human cell cultures, this would have likewise added a few random mutations making the result harder to distinguish as deliberately manipulated. Nevertheless, we know WIV was doing precisely this type of research - creating chimeric coronaviruses and then passaging them.

    While what I've said is consistent with the data presented in the Wuhan lab's correspondence, that is obviously not what they're arguing. They are saying that because that spike protein evolved naturally in RmYN02, a similar spike protein could have evolved naturally in the hypothesized progenitor of SARS-CoV-2. I agree that is also a possibility, but for it to have happened in the wild rather than during passages in a lab, still means that it would have also had to acquire only the receptor binding domain from a pangolin which is far-fetched in my mind, due to the specificity and other logistics reasons already mentioned in the thread.

    Regarding that article you posted, it contains no new relevant information. It cites Andersen et al and the Wuhan Institute of Virology.

    As far as the politics are concerned, I can only say it seems like you're projecting some inversion of your own concerns onto me. The simplistic narratives politicians and hyperpartisans create serve a function for them, but they don't interest me (except from an anthropological perspective), nor do I get shocked every time a politician acts like a politician. The media isn't much better these days. Not that it ever really is when it comes to science, but as soon as Trump opens his mouth on any topic, you can't expect much objectively from them. Trump aligned outlets amplify whereas the rest drive clicks by one dimensionally appealing to their target audience's righteous outrage. Like I said before, truth is not determined by putting a negative sign in front of whatever Trump says anymore than it is by blindly accepting Pompeo's unsupported assertions.

    In my opinion, the best general audience articles on the topic have already been posted in the thread:

    Leaning wild origin: The biggest mystery: what it will take to trace the coronavirus source

    Leaning lab origin: The Case Is Building That COVID-19 Had a Lab Origin

    To me, those two represent the range of reasonable opinions based on the current evidence. Anything more extreme either way seems to be coming from people who either have some other agenda, don't understand the evidence, and/or are talking out their asses.
    Last edited by sumskilz; June 11, 2020 at 05:29 AM.
    Quote Originally Posted by Enros View Post
    You don't seem to be familiar with how the burden of proof works in when discussing social justice. It's not like science where it lies on the one making the claim. If someone claims to be oppressed, they don't have to prove it.


  9. #29
    Ludicus's Avatar Comes Limitis
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    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by sumskilz View Post
    They are saying that because that spike protein evolved naturally in RmYN02, a similar spike protein could have evolved naturally in the hypothesized progenitor of SARS-CoV-2. I agree that is also a possibility, but for it to have happened in the wild rather than during passages in a lab, still means that it would have also had to acquire only the receptor binding domain from a pangolin which is far-fetched in my mind,
    Not really.Pangolin or not Pangolin, that's the question? I have already read the paper, (PDF) Is considering a genetic-manipulation origin for SARS a conspiracy that must be censored?

    Read this- It's wise to presume that 1) the authors don't know what they are talking about. 2) they sold their souls to China (They don't mention a lab origin, I know it looks suspicious).

    SARS-CoV-2 and COVID-19: A genetic, epidemiological, and evolutionary perspective

    ....Both BatCoVs display an average nucleotide identity of ~95% with SARS-CoV-2, although with variations through the genome, and they were detected in bats sampled in Yunnan province, China, in 2019 and 2013, before the first detection of SARS-CoV-2 in humans (Zhou et al., 2020b).

    Both the place and timing of BatCoV RmYN02 and RaTG13 detection, as well as their levels of identity with SARS-CoV-2, indicate that these viruses are not direct progenitors of the SARS-CoV-2 pandemic strain, but clearly support the view that the latter had an ultimate bat origin (Zhou et al., 2020b) (Fig. 1A).

    ....First, most although not all, early COVID-19 detected cases were associated with the Huanan seafood and wildlife market in Wuhan city, where several mammalian species were traded (Huang et al., 2020). This is reminiscent of the circumstances associated with the initial phases of SARS-CoV spread, as palm civets were sold in wet markets and their meat consumed (Cui et al., 2019)

    One possible explanation for this observation is that the RBDs of SARS-CoV-2 and Guangdong pangolin viruses have been progressively optimized through natural selection (convergent evolution) to bind ACE2 molecules from humans and pangolins (and possibly other non-bat mammalian species) (Lam et al., 2020).

    An alternative possibility is that recombination events among coronaviruses hosted by bats, pangolins, and possibly other mammals originated the progenitor of SARS-CoV-2 (Lam et al., 2020; Cagliani et al., 2020).
    It is presently impossible to disentangle these two alternative scenarios, and only the sequencing of additional related sarbecoviruses might eventually clarify the evolutionary history of SARS-CoV-2 RBD.
    It is also worth mentioning here that, as previously noted (Andersen et al., 2020), the similarity of the SARS-CoV-2 RBD with that of viruses only recently sequenced from pangolins can be regarded as a major evidence against the circulating theory that SARS-CoV-2 is the result of deliberate human manipulation.

    In any case, these data do not necessarily imply that pangolins had a role in the emergence of SARS-CoV-2 and in its spread to humans, as these animals might have in turn contracted infection from a bat or other reservoir.

    Moreover, the SARS-CoV-2 spike protein displays a unique feature that is not shared with either BatCoV RaTG13 or the pangolin viruses, namely the presence of a furin cleavage site insertion (PRRA) at the S1-S2 junction (Walls et al., 2020) (Fig. 1D and F). This feature, also absent in SARS-CoV, was suggested to increase viral infectivity and/or pathogenicity (Walls et al., 2020; Andersen et al., 2020).

    It is presently unknown how and when SARS-CoV-2 acquired the furin cleavage site, but it is equally unexplored whether it affects any viral phenotype or if it contributed to adaptation to humans or other hosts. Importantly, though, the presence of a similar insertion in a virus isolated from wild bats is another strong indication in favor of a natural animal origin of SARS-CoV-2 (Zhou et al., 2020a).
    It's not "far-fetched", and certainly not an highly improbable sequence of naturally-occurring coincidences. It is a reasonable explanation.
    Again, there is no evidence that passage experiments played any role in the origin of the coronavirus. Speculations, theories.

    Quote Originally Posted by sumskilz View Post
    As far as the politics are concerned...
    ...More important is the fact that killing the grant was a disgrace. You have a different opinion, those opportunistic Nobel guys and Daszak are not to be trusted, you can even explain it to me in detail, in a very "rational" way of looking at things. You have already did it: three phrases to kill the credibility of everyone involved.I quote," the claim that EcoHealth "lost the ability to look for new viruses in China" is BS...nobody wants to have their grant suspended mid-project...I don't have much sympathy for Daszak due to the lack of integrity" .
    There is no political bias, of course.

    Letter,
    77 US Nobel Laureates in Science.
    May 21, 2020

    Dear Secretary Azar and Director Collins:

    The 77 signatories of this letter, American Nobel Laureates in Physiology or Medicine, Chemistry, and Physics, are gravely concerned about the recent cancellation of a grant from the National Institutes of Health (NIH) to Dr. Peter Daszak at the EcoHealth Alliance in New York.

    We believe that this action sets a dangerous precedent by interfering in the conduct of science and jeopardizes public trust in the process of awarding federal funds for research.
    For many years, Dr. Daszak and his colleagues have been conducting highly regarded, NIH supported research on coronaviruses and other infectious agents, focusing on the transmission of these viruses from animal hosts to human beings.

    Their work depends on productive collaborations with scientists in other countries, including scientists in Wuhan, China, where the current pandemic caused by a novel coronavirus arose. Now is precisely the time when we need to support this kind of research if we aim to control the pandemic and prevent subsequent ones.
    As has now been widely reported, the grant to the EcoHealth Alliance was abruptly terminated by NIH on April 24, 2020, just a few days after President Trump responded to a question from a reporter who erroneously claimed that the grant awarded millions of dollars to investigators in Wuhan.

    Despite the misrepresentation of Dr. Daszak’s grant, despite the high relevance of the studies to the current pandemic, and despite the very high priority score that his application for renewal had received during peer review, the NIH informed Dr. Daszak and his colleagues that the grant was being terminated because “NIH does not believe that the current project outcomes align with the program goals and agency priorities.”

    Such explanations are preposterous under the circumstances. We are scientists who have devoted our careers to research, both in medical and related scientific disciplines that bear on the overall health and well-being of society, as well as fundamental scientific research, much of it supported by NIH and other federal agencies.

    We take pride in our nation’s widely admired system for allocating funds based on expert review and public health needs. The abrupt revoking of the award to Dr. Daszak contravenes these basic tenets and deprives the nation and the world of highly regarded science that could help control one of the greatest health crises in modern history and those that may arise in the future
    ----

    Charles Moore, in the Telegraph, explains the reason why we should take seriously the theory that the virus may be man-made. He explains, "Given the regime's history of lying". Then goes further to say, "The Chinese understand us extremely well. We understand them extremely poorly. For every one westerner who has trouble to learn Mandarin, there are 10,000 Chinese people who have learnt good English".

    Ok, I'm convinced.

    --

    From the news,
    Virologists vigorously debunk new study on origins of the ...
    This latest allegation is from a team of researchers from British and Norway

    They claim the virus' RNA sequence has elements that appear man-made, or artificially inserted, and that their vaccine, Biovacc-19, will take these purported elements into account.

    The paper is nonsense," said Vincent Racaniello, Ph.D., professor of virology at Columbia University. "The manuscript is replete with incorrect science."
    The British and Norwegian researchers, who hailed from St. George's, University of London, and Immunor AS, a biotech company, respectively, did not respond to repeated requests for comment.

    The British/Norwegian study came in wake of comments from former M16 official Sir Richard Dearlove, who recently pointed to a different study touting what is claimed was new evidence that the virus was developed in a Chinese lab. MI6 is the foreign intelligence service of the government of the United Kingdom.

    Experts from around the world were fast and firm in responding to the man-made virus claims -- with the science they provided backing them up.

    No scientist or group of scientists created this virus in a laboratory. That would require insight into [viral] pathogenesis and protein engineering that does not exist," said Robert Garry, Ph.D., virologist at Tulane University.

    The genetic material and genetic changes to the novel coronavirus are "all what you would expect from natural evolution and an animal source," said Amesh Adalja, MD, infectious disease fellow and senior scholar at Johns Hopkins Center for Health Security.

    "There've been multiple rumors and conspiracy theories," he said. "And I do think you'll probably see more."
    Now, many experts are warning that studies like the British-Norwegian one are not only misleading, but also may lead to a dangerous erosion of public trust in scientific institutions.
    Last edited by Ludicus; June 11, 2020 at 07:29 PM.
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  10. #30

    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by Ludicus View Post
    Not really.Pangolin or not Pangolin, that's the question? I have already read the paper, (PDF) Is considering a genetic-manipulation origin for SARS a conspiracy that must be censored?
    I haven't read it, but from the abstract it looks decent:

    The origin of SARS-CoV-2 is still controversial. Comparative genomic analyses have shown that SARS-CoV-2 is likely to be chimeric, most of its sequence being very close to the CoV detected from a bat, whereas its receptor binding domain is almost identical to that of CoV obtained from pangolins. The furin cleavage site in the spike protein of SARS-CoV-2 was previously not identified in other SARS-like CoVs and might have conferred the ability to cross species and tissue barriers. Chimeric viruses can be the product of natural recombination or genetic manipulation. The latter could have aimed to identify pangolins as possible intermediate hosts for bat-CoV potentially pathogenic for humans. Theories that consider a possible artificial origin for SARS-CoV-2 are censored as they seem to support conspiracy theories. Researchers have the responsibility to carry out a thorough analysis, beyond any personal research interests, of all possible causes for SARS-CoV-2 emergence for preventing this from happening in the future.
    They point out a lot of the same issues I have.

    Quote Originally Posted by Ludicus View Post
    Read this- It's wise to presume that 1) the authors don't know what they are talking about. 2) they sold their souls to China (They don't mention a lab origin, I know it looks suspicious).

    SARS-CoV-2 and COVID-19: A genetic, epidemiological, and evolutionary perspective

    It's not "far-fetched", and certainly not an highly improbable sequence of naturally-occurring coincidences. It is a reasonable explanation.
    I consider that a reasonable position to take, as noted in my last post, but there are issues with their argument. They discount RaTG13 as the progenitor based on the fact that it is estimated that it would have taken 20 to 50 years for it to evolve naturally into SARS-CoV-2. However, it could evolve into SARS-CoV-2 in short order if that evolution involved recombination and passage (which they don't consider). As they note, the wet market addresses how species unlikely to come in contact with each other in the wild could have traded viruses and how such viruses could have ended up in Wuhan, but the wet market wasn't actually the origin. They also don't account for how SARS-CoV-2 was already so efficiently adapted to infecting humans when it first appeared.

    Nevertheless, as I said before, if a less human adapted progenitor or peer strain is found in people or older blood samples, it would significantly undermine the lab escape hypothesis. A much closer relative found in nature would likewise do the same. It's possible that wildlife trade is still somehow responsible even if the Wuhan market specifically is ruled out, so evidence of that could turn up.

    Quote Originally Posted by Ludicus View Post
    Again, there is no evidence that passage experiments played any role in the origin of the coronavirus. Speculations, theories.
    There is no solid evidence either way, only circumstantial evidence.

    This is the flow chart from the Nature article. I circled the answers according to the current state of the evidence:

    Spoiler Alert, click show to read: 
    Quote Originally Posted by Ludicus View Post
    From the news,
    Virologists vigorously debunk new study on origins of the ...
    This latest allegation is from a team of researchers from British and Norway
    Looks like more of the same BS from ABC News:

    "The paper is nonsense," said Vincent Racaniello, Ph.D., professor of virology at Columbia University. "The manuscript is replete with incorrect science."

    "It is absolutely 100% impossible that SARS-CoV-2 was made in a laboratory. The elements in the virus, SARS-CoV-2, all came from bat SARS-like CoVs that circulate in nature," Racaniello told ABC News.
    What sort of scientist makes such harsh critiques of a peer-previewed study he hasn't even read? I know he hasn't read it because he's responding to a claim that isn't actually in the paper. 100% impossible, eh? A quick internet search turned up the fact that Racaniello is involved in gain-of-function research himself, and has long been on a crusade against those who suggest it might be dangerous.
    Quote Originally Posted by Enros View Post
    You don't seem to be familiar with how the burden of proof works in when discussing social justice. It's not like science where it lies on the one making the claim. If someone claims to be oppressed, they don't have to prove it.


  11. #31
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    Default Re: The Potential Lab Origin of COVID-19

    As pointed out in the previous article (post 29) absence of evidence might not be evidence of absence. It is unknown how/when CoV-2 acquired the furin cleavage site.
    Coronaviruses have demonstrated a marked capacity to employ homologous recombination. This recombination mechanism had already been described, a long time ago, Recombination, Reservoirs, and the Modular Spike
    It is likely that SARS-CoV-2 is a recombinant CoV generated in nature between a bat-CoV and another coronavirus- in an intermediate animal host.There, in the intermediate host, the virus could have developed the cleavage site.
    Another possibility, the progenitor virus went directly from bats to humans and then developed the cleavage site. Its well known that the MERS-CoV has jumped multiple times from camels to humans, with the correct RBD, but efficient human to human transmission was not established until the acquisition of the furin cleavage site.

    To sum up, the elements needed for CoV-2 are there, part of the natural order of things.

    Could extensive laboratory passage experiments lead to emergence of CoV-2? as far as we know, it is impossible that the O-linked glycan addition site would have emerged without immune pressure, which is obviously absent in cell cultures. Its well know that a number of viruses, including coronaviruses, have evolved to shield their respective envelope glycoproteins with host-derived glycans to prevent antibody recognition of the underlying protein surface. Developing the glycan shield requires evolutionary pressure from an intact immune system, which cultures cell lack.The evolutionary pressure is essential for the selection process. It is just not possible for CoV-2's O-linked glycan to have developed under a typical cell-culture setting.

    Vincent Racaniello, Professor of Microbiology & Immunology, Columbia University, writes, and I agree.
    still the question remains whether it went through an intermediate animal like many other coronaviruses do or whether it went from bats to humans; the only way we can answer that question is by extensive wildlife surveillance, which takes time. It's not man-made; it's not released from a lab; it's not a bioweapon. This is a virus made in nature. Only nature could make a virus with these kinds of properties. There is no question about that and anyone who thinks otherwise is not looking at the science
    For those interested,
    Peter Daszak joins TWiV (This week in Virology) to explain the work of EcoHealth Alliance in surveillance of bats in China for SARS-related coronaviruses to provide the information needed to prevent future pandemics - and why NIH recently withdrew financial support for their work.
    3/6/2020
    Hosts- Vincent Racaniello, Rich Condit, Kat Splinder, Brianne Barker
    Guest- Peter Daszak
    Video here, https://youtu.be/Et3CHcteWNw
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    Default Re: The Potential Lab Origin of COVID-19

    It is likely that SARS-CoV-2 is a recombinant CoV generated in nature between a bat-CoV and another coronavirus- in an intermediate animal host.There, in the intermediate host, the virus could have developed the cleavage site.
    Another possibility, the progenitor virus went directly from bats to humans and then developed the cleavage site. Its well known that the MERS-CoV has jumped multiple times from camels to humans, with the correct RBD, but efficient human to human transmission was not established until the acquisition of the furin cleavage site.
    Can you explain how the virus is apparently very similar to a bat coronavirus, how it jumped to humans, and how it developed to human->human transmission?
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    Default Re: The Potential Lab Origin of COVID-19

    As I said before, there are two possibilities. Without an intermediate host, that's what you are asking? Bat → human? that's how it worked with the Mers-Cov, reread the previous post, it's a well-know fact:
    camel → human,
    When MERS-CoV was first identified, the closest related virus was in bats; however, it has since been recognized that dromedary camels serve as a virus reservoir and potential source for human infections
    Diversity of Middle East Respiratory Syndrome Coronaviruses ...
    Evidence suggests MERS-CoV infection in humans results from continued introductions of distinct MERS-CoV lineages from camels
    Furthermore, as I said before,in addition to the furin cleavage site, an extra-proline is also present,and we know that the addition of such glycans typically occurs under
    immune selection, as mentioned in my previous post.
    Its well know that a number of viruses, including coronaviruses, have evolved to shield their respective envelope glycoproteins with host-derived glycans to prevent antibody recognition of the underlying protein surface. Developing the glycan shield requires evolutionary pressure from an intact immune system, which cultures cell lack.The evolutionary pressure is essential for the selection process. It is just not possible for CoV-2's O-linked glycan to have developed under a typical cell-culture setting.
    From my previous link, "SARS-CoV-2 and COVID-19: A genetic, epidemiological, and evolutionary perspective"

    In little more than four months, we have learned a lot about SARS-CoV-2 and COVID-19. We know that it is a new coronavirus, closely related to those usually found in bats and, quite oddly, in an endangered species, Malayan pangolins. But we do not know how the jump from a yet unknown intermediate species to humans occurred and how the virus was capable of being so easily and efficiently transmitted among individuals of our species. From what we have learned from other zoonotic spillovers, it seems clear that several factors have concurred in this jump, including ecological, cultural, and possible behavioral. We know that recombination is frequent in coronaviruses, including sarbecoviruses, but we do not know whether this process played a significant role in the emergence of SARS-CoV-2 as a new pathogen. All the evidence gathered so far undermines the possibility that the virus was created in, or escaped from, a laboratory proximate to the city where the initial infections were detected.
    ------
    Much better sound and image

    Last edited by Ludicus; June 13, 2020 at 07:59 AM.
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  14. #34

    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by Ludicus View Post
    As I said before, there are two possibilities. Without an intermediate host, that's what you are asking? Bat → human? that's how it worked with the Mers-Cov, reread the previous post, it's a well-know fact:
    camel → human,
    When MERS-CoV was first identified, the closest related virus was in bats; however, it has since been recognized that dromedary camels serve as a virus reservoir and potential source for human infections
    Diversity of Middle East Respiratory Syndrome Coronaviruses ...
    Like most viruses that have just made a species jump, MERS doesn't easily spread human to human. SARS didn't spread easily human to human at first either. One of the reasons SARS-CoV-2 took the world by storm was that when it first appeared in humans it was already highly adapted to infecting our species, one could say almost fine-tuned by the fact that it appears not to have become any more efficient thus far, despite the massive number of transmissions. That's the big mystery.

    Quoting Zhan et al again (emphasis mine):

    The pairwise comparisons of dN and dS, alongside a dearth of signs of emerging adaptive mutations, suggest that by the time SARS-CoV-2 was first detected in late 2019, it was already well adapted for human transmission to an extent more similar to late epidemic than to early-to-mid epidemic SARS-CoV. One possible scenario is that the SARS-CoV-2 outbreak in late 2019 resulted from a bottleneck event similar to the late epidemic SARS-CoV cases that stemmed from a single superspreader who visited Metropole Hotel in Hong Kong, China in late February, 2003 (36). In comparison to the SARS-CoV epidemic, the SARS-CoV-2 epidemic appears to be missing an early phase during which the virus would be expected to accumulate adaptive mutations for human transmission. However, if this were the origin story of SARS-CoV-2, there is a surprising absence of precursors or branches emerging from a less recent, less adapted common ancestor among humans and animals. In the case of SARS-CoV, the less human-adapted SARS-CoV progenated multiple branches of evolution in both humans and animals (Figure 1, Figure 5). In contrast, SARS-CoV-2 appeared without peer in late 2019, suggesting that there was a single introduction of the human-adapted form of the virus into the human population. This has important implications regarding the risk of SARS-CoV-2 re-emergence in the near future and the severity of its consequences.

    It is important to recall that there were two SARS-CoV outbreaks in 2002-2004, each arising from separate palm civet-to-human transmission events (Figure 5): the first emerged in late 2002 and ended in August, 2003; the second arose in late 2003 from a lingering population of SARS-CoV progenitors in civets. The second outbreak was swiftly suppressed due to diligent human and animal host tracking, informed by lessons from the first outbreak (37,38). To prevent similar consecutive outbreaks of SARS-CoV-2 today, it is vital to learn from the past and implement measures to minimize the risk of additional SARS-CoV-2-like precursors adapting to and re-emerging among humans. To do so, it is important to identify the route by which SARS-CoV-2 adapted for human transmission. However, there is presently little evidence to definitively support any particular scenario of SARS-CoV-2 adaptation. Did SARS-CoV-2 transmit across species into humans and circulate undetected for months prior to late 2019 while accumulating adaptive mutations? Or was SARS-CoV-2 already well adapted for humans while in bats or an intermediate species? More importantly, does this pool of human-adapted progenitor viruses still exist in animal populations? Even the possibility that a non-genetically-engineered precursor could have adapted to humans while being studied in a laboratory should be considered, regardless of how likely or unlikely (39).
    Of course if there are progenitors out there that would prove my suspicions wrong, it is absolutely imperative that they be found.

    From Fernando Castro-Chavez's ResearchGate profile:



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    Quote Originally Posted by Enros View Post
    You don't seem to be familiar with how the burden of proof works in when discussing social justice. It's not like science where it lies on the one making the claim. If someone claims to be oppressed, they don't have to prove it.


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    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by Ludicus View Post
    As I said before, there are two possibilities. Without an intermediate host, that's what you are asking? Bat → human? that's how it worked with the Mers-Cov, reread the previous post, it's a well-know fact:
    camel → human,
    When MERS-CoV was first identified, the closest related virus was in bats; however, it has since been recognized that dromedary camels serve as a virus reservoir and potential source for human infections
    Diversity of Middle East Respiratory Syndrome Coronaviruses ...
    Yes, how did it jump from bats to humans, when the relevant bat habitat is apparently hundreds of miles away?
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    Default Re: The Potential Lab Origin of COVID-19

    Like most viruses that have just made a species jump, MERS doesn't easily spread human to human. SARS didn't spread easily human to human at first either. One of the reasons SARS-CoV-2 took the world by storm was that when it first appeared in humans it was already highly adapted to infecting our species, one could say almost fine-tuned by the fact that it appears not to have become any more efficient thus far, despite the massive number of transmissions.
    SARS1 outbreak started in November 2002 but got identified precisely a few months after (the exact virus I mean). The second outbreak in March and April is probably the moment it became more infectious. Only a few months passed.

    In the case of the current SARS-CoV-2, there is still doubt about dating its origin. A retrospective analysis of scans suggested that some people were infected by the SARS-CoV-2 in France by mid-November 2019. The uncertainties are big enough to make me doubt this particular argument.
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  17. #37

    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by Genava View Post
    SARS1 outbreak started in November 2002 but got identified precisely a few months after (the exact virus I mean). The second outbreak in March and April is probably the moment it became more infectious. Only a few months passed.

    In the case of the current SARS-CoV-2, there is still doubt about dating its origin. A retrospective analysis of scans suggested that some people were infected by the SARS-CoV-2 in France by mid-November 2019. The uncertainties are big enough to make me doubt this particular argument.
    That wasn't a formal study as far as I know. It was a press release that indicated that two scans were found that were compatible with having been COVID-19. If there's more to it, I'm interested, but it doesn't seem like much evidence on its own. The first confirmed case in France was at the very end of December 2019, but if those scans were really COVID-19 cases, that would make them contemporaneous with the first confirmed cases in China, so not necessarily a major timeline shift with air travel and all. SARS-CoV-2 was more well adapted to human transmission when it it was first discovered than SARS-CoV was at the end. The time frame would have to be set back at least six months, probably much more, I would think anyway.

    The difference I'm referring to is pretty drastic:

    Several reports have noted that SARS-CoV-2 appears genetically stable and not under much pressure to adapt, which bodes well for diagnostics, vaccine, and therapeutics development (1–4)...

    To gain a better understanding of how stable the SARS-CoV-2 genome is, we first performed a side-by-side comparison of evolutionary dynamics between SARS-CoV-2 and SARS-CoV. For this analysis, we curated high quality genomes spanning ~3-month periods for the following groups: 11 genomes for early-to-mid epidemic SARS-CoV, 32 genomes for late epidemic SARS-CoV, and 46 genomes for SARS-CoV-2 that included an early December, 2019 isolate, Wuhan-Hu-1, and 15 randomly selected genomes from each month of January through March, 2020 sampled from diverse geographical regions (methods in Supplementary Materials). We were surprised to find that SARS-CoV-2 exhibits low genetic diversity in contrast to SARS-CoV, which harbored considerable genetic diversity in its early-to-mid epidemic phase (Figure 1) (12); nucleotide diversity estimates (13,14) across all sites, non-synonymous and synonymous, for each locus examined are provided in the Supplementary Table.

    SARS-CoV was observed to adapt under selective pressure that was highest as it crossed from Himalayan palm civets (intermediate host species) to humans and diminished towards the end of the epidemic (15–18); this series of adaptations between species and in humans culminated in a highly infectious SARS-CoV that dominated the late epidemic phase. In comparison, SARS-CoV-2 exhibits genetic diversity that is more similar to that of late epidemic SARS-CoV (Figure 1, Supplementary Table). In fact, the exceedingly high level of identity shared among SARS-CoV-2 isolates makes it impractical to model site-wise selection pressure. As more mutations occur and, ideally, when SARS-CoV-2-like viruses from an intermediate host species are identified, it will become possible to model selection pressure as was done for SARS-CoV.

    An examination of 43 SARS-CoV and 46 SARS-CoV-2 genomes revealed a striking difference in the number of substitutions over similar 3-month periods (Figure 1A), with more genetic polymorphism in early-to-mid epidemic SARS-CoV compared to late epidemic SARS-CoV or SARS-CoV-2 (Figure 1B). To rule out a subsampling artefact, we performed one hundred sampling experiments from all high-quality SARS-CoV-2 sequences on GISAID; IQtree phylogenies were built from the one hundred 46-taxon subsampled sequence sets, i.e., 15 randomly selected samples from each month of January through March, 2020 from diverse geographical regions, in addition to Wuhan-Hu-1. The maximum tip-to-tip distance (number of substitutions between two genomes) of the early-to-mid epidemic SARS-CoV tree (~85 substitutions) was greater than that of all one hundred resampled SARS-CoV-2 trees (~15-25 substitutions; p < 0.01). Even by April 28, 2020, the SARS-CoV-2 genomes available on GISAID spanning 4 months exhibited modest genetic diversity (Supplementary Figure 1) as compared to early-to-mid epidemic SARS-CoV.

    Numerous adaptive mutations that evolved in SARS-CoV S RBD have been experimentally demonstrated to enhance binding to the human ACE2 receptor and facilitate cross-species transmission, e.g., residues N479 and T487 (29,30), as well as K390, R426, D429, T431, I455, N473, F483, Q492, Y494, R495 (31); or predicted to have been positively selected, e.g. residues 239, 244, 311, 479, 778 (17) (Figure 3). In contrast, the majority of the non-synonymous substitutions in SARS-CoV-2 S are distributed across the gene at low frequency and have not been reported to confer adaptive benefit (Figure 4). Yet, the SARS-CoV-2 S has been demonstrated to bind more strongly to human ACE2 and has a superior plasma membrane fusion capacity compared to the SARS-CoV S (32,33). The only site of notable entropy in the SARS-CoV-2 S, D614G, lies outside of the RBD and is not predicted to impact the structure or function of the protein (34). Its prevalence in international COVID-19 cases has been attributed to the substitution occurring early in the pandemic leading to a founder’s effect. There is no evidence of a more virulent strain of SARS-CoV-2 emerging despite passage through more than 3 million human hosts by the time of this analysis.
    Caveat regarding the last sentence, this preprint argues that D614G which evolved in Europe is more virulent, but so far that is not a widely accepted view (for example). Although I don't think it would make a difference to the mystery since early SARS-CoV-2 would still be better adapted to infecting humans than late SARS-CoV was. Considering the massive number of transmissions, if SARS-CoV-2 weren't already fine-tuned for infecting humans, we would expect to see rapid evolution.

    Also:

    SARS-CoV-2, but not SARS-CoV, replicated modestly in U251 (neuronal) cells (p=0·036). For animal species cell tropism, both SARS-CoV and SARS-CoV-2 replicated in non-human primate, cat, rabbit, and pig cells. SARS-CoV, but not SARS-CoV-2, infected and replicated in Rhinolophus sinicus bat kidney cells. SARS-CoV-2 consistently induced significantly delayed and milder levels of cell damage than did SARS-CoV in non-human primate cells (VeroE6, p=0·016; FRhK4, p=0·0004)...

    SARS-CoV-2 has been postulated to originate from R sinicus bats, because the virus is phylogenetically most closely related to coronaviruses found in these bats.26 Our findings raise the possibility that SARS-CoV-2 has already adapted well to humans and, thus, the virus is no longer able to propagate well in R sinicus bat cells, providing a possible explanation for the efficient person-to-person transmission of COVID-19.
    Quote Originally Posted by Enros View Post
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    Default Re: The Potential Lab Origin of COVID-19

    Well, there is no roadmap in the virus genome telling it how to became the perfect virus for the human body in a several months. It is hard to argue if there was enough or not enough time to get the mutations involved in its increasing transmission human-to-human, because those are random processes. It is logical that the virus doesn't have a large diversity once it gets a good infection rate because mutations have most chances to reduce its effectiveness than increase it.

    Quote Originally Posted by SARS-CoV-2: Combating Coronavirus Emergence
    Andersen et al. also argue that it is possible that a progenitor coronavirus jumped to humans prior to acquiring its polybasic site and key hACE2 interaction residues, acquiring these features through undetected human-to-human transmission events prior to the first documented cases of COVID-19 disease that triggered human surveillance systems (Wu et al., 2020, Zhou et al., 2020). In support, antibodies targeting the group 2b SARS-like coronaviruses can be detected in people living and working near or in bat hibernacula in China, suggesting frequent exposures in a rural setting. As SARS-CoV-2 infections are frequently asymptomatic or mild, initial exposures would easily have allowed for extended silent transmission events in rural settings prior to the emergence of a strain that could support sustained human-to-human transmission, especially when brought into an urban setting.
    Furthermore Andersen et al. already argued in its March publication against the possibility of an inadvertent cell culture origin.

    Quote Originally Posted by The proximal origin of SARS-CoV-2
    Basic research involving passage of bat SARS-CoV-like coronaviruses in cell culture and/or animal models has been ongoing for many years in biosafety level 2 laboratories across the world, and there are documented instances of laboratory escapes of SARS-CoV2. We must therefore examine the possibility of an inadvertent laboratory release of SARS-CoV-2.

    In theory, it is possible that SARS-CoV-2 acquired RBD mutations (Fig. 1a) during adaptation to passage in cell culture, as has been observed in studies of SARS-CoV. The finding of SARS-CoV-like coronaviruses from pangolins with nearly identical RBDs, however, provides a much stronger and more parsimonious explanation of how SARS-CoV-2 acquired these via recombination or mutation.

    The acquisition of both the polybasic cleavage site and predicted O-linked glycans also argues against culture-based scenarios. New polybasic cleavage sites have been observed only after prolonged passage of low-pathogenicity avian influenza virus in vitro or in vivo. Furthermore, a hypothetical generation of SARS-CoV-2 by cell culture or animal passage would have required prior isolation of a progenitor virus with very high genetic similarity, which has not been described. Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described. Finally, the generation of the predicted O-linked glycans is also unlikely to have occurred due to cell-culture passage, as such features suggest the involvement of an immune system.
    I found deeper explanation made by Christian Stevens from the Benhur Lee Lab:

    But what if this virus was developed using simulated natural selection in a lab?

    This is a good question and one we can answer in a few ways.

    First, the likelihood of simulated natural selection stumbling on the near exact RBD from a previously unknown pangolin coronavirus is mathematically unlikely. Much less likely than simply stealing it from the pangolin coronavirus via recombination in nature.

    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.

    Natural or Unnatural Selection: The Ka/Ks Ratio

    The Ka/Ks ratio gives us powerful insight into the history of anything with a genome. Before using it to asses SARS-CoV-2, we first need a quick biology intro to the types of mutations a genome can experience. Here’s what you need to know:

    => Many mutations to a genome won’t actually result in a functional change (synonymous mutations)

    => Some mutations to the genome will result in a functional change (non-synonymous mutations)

    => By comparing the number of synonymous and non-synonymous mutations, we can infer the type of selective pressure that occurred

    Because synonymous mutations should have no effect, we expect them to happen at a relatively consistent rate. That makes them a good baseline that we can compare the number of non-synonymous mutations to. By calculating the ratio between these two numbers we can differentiate between three different types of selection:

    1. Purifying selection: This virus is already a great fit where it is and cannot afford to change because every change makes it worse. You should see very few non-synonymous changes here.

    2. Darwinian selection: This virus is not a good fit where it is and has to change and get better or it’s going to die out. You should see many non-synonymous changes.

    3. Neutral selection: There is no pressure on this virus either way. Non-synonymous changes and synonymous changes should come at about the same rate.

    We would expect a virus that is learning to exist in a new context would be undergoing Darwinian selection and we would see a high rate of non-synonymous changes in some part of the genome. This would be the case if the virus were being designed via simulated natural selection, we would expect at least some part of the genome to show Darwinian selection.

    In an analysis by Dr. Trevor Bedford using an open-source program (that you can try at home), he began with the sequences of all viruses related to SARS-CoV-2. He next calculated the Ka/Ks ratios when comparing SARS-CoV-2 to related viruses. He also calculated the Ka/Ks ratio for SARS-CoV-2 to a hypothetical ancestor virus predicted by his program. In his analysis, Dr. Bedford found that 14.3% of the mutations between SARS-CoV-2 and its predicted ancestor resulted in non-synonymous mutations. RaTG13, a natural coronavirus has 14.2% of its mutations as non-synonymous. Both of these numbers indicate a purifying selection, with very few non-synonymous changes. This holds true across the entire genome with no part of it showing Darwinian selection. This is a very strong indicator that SARS-CoV-2 was not designed using forced selection in a lab.
    https://leelabvirus.host/covid19/origins-part3
    LOTR mod for Shogun 2 Total War (Campaign and Battles!)
    https://www.youtube.com/watch?v=bIywmAgUxQU

  19. #39

    Default Re: The Potential Lab Origin of COVID-19

    Quote Originally Posted by Genava View Post
    Well, there is no roadmap in the virus genome telling it how to became the perfect virus for the human body in a several months. It is hard to argue if there was enough or not enough time to get the mutations involved in its increasing transmission human-to-human, because those are random processes.
    The more specific you want to get, the harder it is to argue with any certainty. Nevertheless, estimates are made all the time regarding how long it would take for something to evolve naturally based on mutation rate, population size, and the selection coefficient of particular traits. This is precisely the reason those who are highly skeptical of the Wuhan lab being the source of COVID-19 argue that RaTG13 cannot be the progenitor, and I agree with them when it comes to unguided selection. But that's not really the main issue, SARS-CoV-2 appeared suddenly with multiple features that lead to improved infectivity in humans already in place. How did it remain undetected in its previous stages of evolution? It had to be spreading in humans if it was becoming fine-tuned to spreading in humans. The circumstances are completely unlike any other disease that has been carefully studied in ways that appear not to make evolutionary sense, at least given the current state of the data.

    Quote Originally Posted by Genava View Post
    It is logical that the virus doesn't have a large diversity once it gets a good infection rate because mutations have most chances to reduce its effectiveness than increase it.
    Purifying selection can't operate on synonymous mutations since they literally have no effect. Nevertheless, these mutations are valuable for phylogeny. Take for example the codon CCU which codes for proline, any point mutation in that third nucleotide has no effect, because CCC, CCA, and CCG likewise code for proline. There are two to four possible combinations for every amino acid. Due to the size of its massively expanding reproductive pool, SARS-CoV-2 rapidly became diverse, but only where it didn't matter. Its phylogeny can be traced back to a single source that was already highly adapted to infecting people.

    Purifying selection can't create a single strain without peers or progenitors. If peers and progenitors are out there, they haven't been found.

    Quote Originally Posted by Genava View Post
    Furthermore Andersen et al. already argued in its March publication against the possibility of an inadvertent cell culture origin.
    I already addressed Andersen et al, but here is Rossana Segreto's response to that among some of their other arguments.:

    For Andersen and colleagues,49 strong evidence that SARS-CoV-2 did not result from genetic manipulation is that the high-affinity binding of the SARS-CoV-2 spike protein to hACE2 could not have been predicted by models based on the RBD of SARS-CoV. Based on the structural analysis conducted by Wan and colleagues,50 SARS-CoV-2 has the potential to recognize hACE2 more efficiently than the SARS-CoV which emerged in 2002. Moreover, generation of CoV chimeric strains has recently demonstrated that bat CoV spikes can bind to the hACE2 receptor with more plasticity than previously predicted.16 All amino acids in the RBD have been extensively analysed and new models to predict ACE2 affinity are available.51 As described above, creation of chimeric viruses has been carried out over the years with the purpose to study the potential pathogenicity of bat CoVs for humans. In this context, SARS-CoV-2 could have been synthesized by combining a backbone similar to RaTG13 with the RBD of CoV similar to the one recently isolated from pangolins13, because the latter is characterized by a higher affinity with the hACE2 receptor. Such research could have aimed to identify pangolins as possible intermediate hosts for bat-CoV potentially pathogenic for humans.

    Regarding the furin cleavage site, Andersen and colleagues49 state that “The functional consequence of the polybasic cleavage site in SARS-CoV-2 is unknown”. New studies from several groups have lately identified this activation site as possibly enabling the virus to spread efficiently between humans and attack multiple organs.52 Experiments on proteolytic cleavage of CoV spike proteins have been recently suggested as future key studies to study virus transmissibility in different hosts. 51 The pangolin from which MP789 was isolated was co-infected by several viruses13, among others the Herpes Virus that is characterized by a furin cleavage site. In a context of an evolutionary study, this observation might have suggested the idea of this insertion into SARS-CoV-2.

    Andersen and colleagues49 also state, based on the work of Almazan and colleagues53 that “the genetic data irrefutably show that SARS-CoV-2 is not derived from any previously used virus backbone”. In the last six years before the outbreak of SARS-CoV-2 the number of potential bat backbones has been undeniably increased by several bat CoV screenings, last but not least bringing RaTG13 to scientific attention in January 2020. Other possible backbones could, as well, still wait for publication.

    Andersen and colleagues49 also state that “The acquisition of both the polybasic cleavage site and predicted O-linked glycans also argues against culture-based scenarios”. Methods for insertion of a polybasic cleavage site in infectious bronchitis CoV are given in Cheng and colleagues54 and resulted in increased pathogenicity. Concerning the predicted O-linked glycans around the newly inserted polybasic site, it should be noted that this prediction was not confirmed by Cryo-EM inquiry into the SARS-CoV-2 spike glycoprotein.55 Nevertheless, while it is true that O-linked glycans are much more likely to arise under immune selection, they could be added in the lab through site-directed mutagenesis56 or arise in the course of in vivo experiments, for example, in BLT-L mice that have human lung implants and autologous human immune system57 or in mice expressing human ACE2 receptor.58 To overcome problems of bat CoV isolation, experiments based on direct inoculation of bat CoV in suckling rats have been carried out.59 Pangolins or other animals with similar ACE2 conformation could have been used as experimental animals as well. The authors also state that “Subsequent generation of a polybasic cleavage site would have then required repeated passage in cell culture or animals with ACE2 receptors similar to those of humans, but such work has also not previously been described.” It should not be excluded that such experiments could have been aborted due to the SARS-CoV-2 outbreak, before a possible publication of the results or that the results were never intended to be published.
    Regarding the last part, it actually was described (referenced earlier in the thread). In the Daszak/WIV research grant proposal if I remember correctly.

    Quote Originally Posted by Genava View Post
    I found deeper explanation made by Christian Stevens from the Benhur Lee Lab:
    Quoting from the second part of this argument:

    We would expect a virus that is learning to exist in a new context would be undergoing Darwinian selection and we would see a high rate of non-synonymous changes in some part of the genome. This would be the case if the virus were being designed via simulated natural selection, we would expect at least some part of the genome to show Darwinian selection.
    Yes, we sure would, but not only would that be true for simulated natural selection, it would be true for natural selection as well, such as when a virus is learning to exist in a new species. How is this an argument against lab origin?

    I'm going to really drive this home:

    In his analysis, Dr. Bedford found that 14.3% of the mutations between SARS-CoV-2 and its predicted ancestor resulted in non-synonymous mutations. RaTG13, a natural coronavirus has 14.2% of its mutations as non-synonymous. Both of these numbers indicate a purifying selection, with very few non-synonymous changes. This holds true across the entire genome with no part of it showing Darwinian selection.
    He literally just argued that no part of the SARS-CoV-2 genome shows signs of Darwinian selection.

    So let's accept that claim as true, and say there has been no Darwinian selection since SARS-CoV-2's predicted ancestor. That would mean its predicted ancestor was just as virulent in humans as SARS-CoV-2. How would such a virus exist in humans without detection? How would such a virus become so fine-tuned to infecting humans if it wasn't in humans? I have a hypothesis that explains how the latter could happen, but so far I've yet to hear a plausible alternative explanation.
    Last edited by sumskilz; June 18, 2020 at 04:01 PM. Reason: fixed formatting issues in quote
    Quote Originally Posted by Enros View Post
    You don't seem to be familiar with how the burden of proof works in when discussing social justice. It's not like science where it lies on the one making the claim. If someone claims to be oppressed, they don't have to prove it.


  20. #40
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    Default Re: The Potential Lab Origin of COVID-19

    The Anglosphere- as in the society and government- has been anti science for such a long time that they disregard scientific evidence that contradicts the political 2 minute hate of the day.

    And nowhere is this most apparent than in the dismissal of evidence when it contradicts the desire to blame all of one's problems on China.

    QAnon proponents better start asking their inane low IQ questions to these italian scientists, and please, something other than "tHeY wUz Paid bY cHiNa"

    Coronavirus was already in Italy by December, waste water study finds

    Italian scientists say sewage water from two cities contained coronavirus traces in December, long before the country's first confirmed cases. The National Institute of Health (ISS) said water from Milan and Turin showed genetic virus traces on 18 December.
    It adds to evidence from other countries that the virus may have been circulating much earlier than thought.
    Chinese officials confirmed the first cases at the end of December. Italy's first case was in mid-February.
    In May French scientists said tests on samples showed a patient treated for suspected pneumonia near Paris on 27 December actually had the coronaviru
    Source: https://www.bbc.com/news/world-europe-53106444

    The European strains are older than the strains found in Wuhan. Now, i know that this is going to go against the 2 minute hate that white anglo society indulges in but when something is found to be older, it stands to reason that it was occurring before the newer strain, even the one in Wuhan. We have this wonderful technology called genetics to be able to verify this.

    Whilst it is unfortunate that european farming is going to suffer from this, at least we now know that wildlife markets in Wuhan was not the progenitor of SARS-Cov-2, and that the virus can survive in sub zero temperatures for a lengthy period of time.
    Last edited by Exarch; June 19, 2020 at 09:15 AM.

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