Not to mention that they are no longer amino acids in the context of the protein, but residues.
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This is so confused that it is hard to know where to start.
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I have a hard time following many of the elements of the Lab Leak Theory. For instance, some people make a big deal about the claim that WIV had a database of viruses that was taken off-line in Sept, 2019, three months before the first cases of COVID-19 were reported.
OK, so what? Is the claim here that the lab knew one of their viruses had leaked into the public and was about to cause a global pandemic three months into the future? If not, what is the claim?
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I disagree with you for even if you replace the spike protein of a dangerous coronavirus able to infect human cells with a bat spike protein, there is no absolute guarantee that the new chimeric virus wonât be still more dangerous, even if, I grant you, such an outcome would be highly unlikely.
I am not sure to understand what you mean by pseudovirus. Anyhow, the new chimeric viruses created by the WIV researchers were tested for their ability not only to replicate in human airway cells but also to replicate and caused pathogenesis in mouse model.
If it was the case that the covid19 pandemic was caused by a leak from a lab doing gain of function studies, it would be stupid to pursue this kind of research. Here is an interesting piece regarding this point:
Looking forward to Prof. Racanielloâs explanations to some of these later this week:
TimestampsâŚ
Nicholas Wade to be rebutted by Racaniello later
4:40 â 5:40
China animal surveillance
10:00 â 12:45
GoF research and lab-leak
22:10 â 24:45 | 37:35 â 37:52 | 48:50 â 49:20 | 55:05 â 57:14 | 1:09:00 â 1:10:20
Indian variant more transmissible?
57:35 â 1:01:20
*Im not sure that Vincent is accurate about his âfitnessâ argument. I understand that some others agree with him, but why would so many others disagree. I guess itâs a complex subject.
No confusion about the statement being flat out wrong⌠âBreathtakingly wrong and shocking to read from someone who should absolutely know itâs wrongâ, is a better description. The sort of thing that would justify your thesis committee in not granting your scientific degree.
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Yikes â thatâs about the worst assessment of the transmissibility of SARS-CoV-2 variants Iâve seen.
OkayâŚHow come?
Unfortunately I think you can object away basically any and all genetics research with these kinds of what ifs placed on a foundation of you canât predict everything.
It can mean different things depending on the use, but generally often times it means a part of a virus (such as a spike protein), or a relatively intact virus rendered incapable of replicating. Replication incapable retroviruses for example, are used routinely in all sorts of research to deliver genes to cells.
Yes. The already existing virus capable of infecting human cells with itâs bat spike protein in replacement of the one it had. That seems like a sensible experiment to do because that experiment would then tell something about whether the bat virus was capable of infecting human cells if it underwent reassortment with another virus.
Unfortunately that article is based on the premise that something was made more dangerous than it already was. And it presents a false dichotomy:
If, on the other hand, Covid-19 is Mother Natureâs handiwork, then logically we are condemned to a sequence of pandemics; some natural, others accidental, some better and others far more deadly.
No, itâs not âon the other handâ. Even if Covid-19 is a lab-leak, we are STILL condemned to a sequence of future natural pandemics. Evoution doesnât abide by human conventions, and genetic mutations and reassortments among natural viruses will occur regardless, and we will have no idea what to look out for. Someone is going to have to investigate the methods viruses use to infect and cross to other species, try to understand it as best we can, so we can both better predict where they are likely to happen so we can take cost-effective precautions (we canât monitor everything at maximum level of dilligence, we will have to prioritize things more likely to be dangerous than others less likely to be dangerous), so we can develop better drugs against them, and so we might even have a head start for future vaccine developments.
And nobody is âturbo-charging viruses in the labâ. I think we can agree nobody should be âturbo-chargingâ replication-capable viruses in the lab. But as far as we know, thatâs not what has happened here. None of the experiments we know about having taken place at the WIV can be meaningfully said to constitute âturbo-charging viruses in the labâ.
I also have to say Bret Weinstein is quite a bullshitter, writing:
Either is possible. Yet despite incredible pressure for the Chinese government to find it, so far there is no evidence of a plausible ancestor virus having circulated in an intermediate population. When SARS2 first appeared in Wuhan in late 2019, it was, from the very first moment, pre-adapted to spread through the human body and from one person to another. Thatâs all but impossible â a major evolutionary mystery.
No, itâs not âall but impossibleâ, and thereâs no sense in which it is âpre-adaptedâ to spread through he human body or from one person to another, any more than itâs âpre-adaptedâ to spread through the body of a mink, and from one mink to another, and thatâs no goddamn mystery. Mammals have many physiological and cellular, molecular similarities that allow for the possibility of successful generalist viruses. Heck, weâre some times hit by BIRD-flus.
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Then I am sure that you donât understand what is absurd about the false accusations you are relaying.
Gill, your response went off the rails. According to the study featuring Zheng Li that Wade cited in his article, the chimeric SCH014-MA15 ( SCH014 represents the spike protein of SCH014-CoV, while MA15 is the backbone; MA15 is mouse-adapted SARS-CoV ) virus wasnât more dangerous than wild-type SARS-CoV (both the human- and mouse-adapted strains). Take a look at the charts yourself (graphs c & d; SCH014-MA15 is represented by the green line, while wild-type SARS-CoV {the human-adapted strain, also called SARS-CoV Urbani} is represented by the black line):
In graphs c & d, we see that just like SARS-CoV Urbani, the chimeric SCH014-MA15 showed robust replication in Calu-3 2B4 and HAE (both human) cells). Both viruses had similar titers or concentrations following infection.
Also look at graph e and compare the percentage weight loss caused by the chimeric virus (green line) versus the mouse-adapted SARS-CoV (or SARS-CoV MA15 or MA15; black line). Its obvious that despite having similar viral titers to MA15 (see graph f), it did not produce comparable weight loss or death in infected mice indicating it was somewhat attenuated in those mice.
The researchers also looked at the SCH014-CoV itself. Guess, what? It could also infect human cells as well, but unlike SARS-CoV, it did this poorly. More graphs for you:
Fix your eyes on graph c above: SCH014-CoV (green) was able to infect human (HAE: Human Airway Epithelial) cells, but it was attenuated relative to SARS-CoV (black) which showed robust replication. This tells us even if SCH014-CoV could pass on to someone who came close to a bat that had it, but without further adaptations like those found in its sister SARS-CoV, it most likely would not cause any serious outbreak. It might succeed at infecting a few people, but will burn out eventually. Thatâs the sort of foresight we get from this kind of research.
I hope you can now see why Rum said the chimeric virus wasnât more dangerous relative to wild-type SARS-CoV Urbani (human-adapted SARS-CoV) or wild-type MA15 (mouse-adapted SARS-CoV).
Can chimeric viruses be more dangerous than their parental types? Yes. For example, MA15 with SARS-CoV Urbani spike protein is not as pathogenic as MA15 with SCH014 spike protein. However, you can only know and prepare for this either via experimentation under safe conditions in some lab or after some months after another outbreak usually thrown our way by nature, because nature regularly creates virus chimeras.
Nope. Its you who doesnât understand what a pseudovirus means. Pseudoviruses replicate once intracellularly and lack virulence factors present in their parents, making them safe to work with.
I disagree. @Rumraket response mirrors whatever I would have penned down here.
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I am not accusing anyone here, but just expressing the idea that the lab leak scenario is a plausible hypothesis that should be thoroughly investigated.
Of course not, none of us were working at the WIV, or have a position that would involved a cover-up. However, you are making accusations that multiple people are either completely lying, or are covering up for those that are.
I donât think anyone here has disagreed with that. Regardless, you continue to argue for the lab leak that everyone says is plausible, but not as likely as natural origin.
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Okay, let me clarify my view, the same as Wadeâs, which is that the laboratory leak hypothesis is not only plausible but also more convincing than the natural origin hypothesis.
I can see that this is not a majority view on this site. Thatâs okay. Letâs agree to disagree.
No, letâs agree that, as is your habit, you are adopting a position that is directly contradicted by the totality of available evidence, but you are either unable or unwilling to accept this.
OK?
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The only thing going for a lab leak is Chinaâs lack of transparency and unwillingness to allow unhindered probe of the WIV, but its not surprising that China is behaving this way. So for a natural emergence, nothing about the molecular features of the virus or even Chinaâs attitude to international calls for a transparent probe clashes with it. It is the most likely explanation for the origin of SARS-CoV-2.
It is not the majority view because it lacks the same measure of support available for a natural emergence. However, until we find SARS-CoV-2âs closest relative in the wild, a lab leak remains a possibility even if its an extremely unlikely one.
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Wadeâs view is based on misrepresenting evidence. Your view involves ignoring the evidence and users Wadeâs misrepresentations to make false accusations.
You have posted many false claims and accusations regarding COVID-19 and itâs treatment here.
Please stop. Please examine the evidence BEFORE coming to conclusions. It is the responsible and ethical thing to do.
Directly contradicted by the totality of available evidence? You should say that to Robert Redfield, an eminent virologist and former CDC director.
While I would disagree with the exaggerated characterization given by @Faizal_Ali above (I donât so much think the lab-leak hypothesis is contradicted so much as it is basically just unsupported by the evidence), I also have to say I find your never-ending milking of the appeal to âeminentâ authorities cringe-worthy.
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Redfieldâs comments donât advance the discussion of SARS-CoV-2 origins, as they are unrooted in any evidence (by his own admission) and plagued by an apparent faulty understanding of basic virology. Broadly speaking, Redfield finds it implausible for a virus to jump from a bat to humans and immediately be as contagious as SARS-CoV-2. Rather, he thinks the virus was manipulated in the lab through a process called serial passage and became better adapted for human transmission.
Itâs often stated almost as a truism, and apparently accepted by Redfield, that a virus crossing from animals into people has to undergo rapid adaptation to become transmissible in humans. While that may often be true, it doesnât have to be. We know SARS-CoV-2 itself can jump seamlessly between hosts â itâs gone multiple times from humans into minks and spread like wildfire. It transmits perfectly well among hamsters and ferrets in the lab. If a human virus can transmit among mink, thereâs no basis to assume a bat virus canât transmit among humans. Us humans may think weâre very special â but to a virus we are just another mammalian host.
That said, itâs undoubtedly true that any virus finding itself in a new host will adapt to new surroundings, and SARS-CoV-2 is no different. And maybe Redfield is right that this is an instance in which the virus circulating in animals wouldnât have been immediately efficient at human-to-human transmission. In that case, the virus would have to adapt quickly in humans and it would have had to do so before it was discovered by Chinese scientists in late December 2019. Did it have the chance then? A powerful recent study in Science estimated that SARS-CoV-2 first started circulating in Wuhan between mid-October and mid-November 2019, one or two months for it to circulate at a low level and adapt to a new host â us. But did it adapt? Another recent study, not yet peer-reviewed, identified a single mutation in the SARS-CoV-2 spike gene that probably occurred in those one to two months. These seemingly missing evolutionary links that led Redfield down the road to a lab accident are being filled by real scientific data in front of our eyes.
Redfieldâs more sinister claim â that Chinese researchers passaged this virus repeatedly to make it grow better and thus adapted it to human transmission in the lab â simply doesnât hold up. A study from late 2020 in PLoS Biology demonstrated that the ability of SARS-related coronavirus spike proteins to bind to human cells is naturally evolving in the viral milieu, and a more recent not-yet-peer reviewed study found that SARS-CoV-2 isnât even unusually good at doing so; the spike of a closely related virus found in pangolins initiates infection of human cells much more effectively. SARS-CoV-2 is still adapting though. The spike protein from the B.1.1.7 variant acts a lot more like the pangolin virus spike protein. Evolution never stops.
More fundamentally, adaptation to human transmission and virulence is exactly the opposite of what weâd expect from serial passage in cells or animals. This exact process is a classic way of weakening a virus to make a vaccine â the oral polio vaccine developed by Sabin and the yellow fever vaccine have used this approach, among many others. Thatâs because viruses evolve virulence and transmission in a complex host system. If you extract them from that system and force them to evolve in a different context (like in cells outside a body) they âde-adaptâ to the âreal world,â precisely the opposite of what Redfield suggests. Frankly, itâs hard to understand why he wouldnât know that.
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