Evidence it was a lab leak? (weapon, crime, economy, votes)

These next posts were also posted in another thread on this subject:

Again, not much meaningful rebuttals so lets move onto the "Natural selection in an animal host before zoonotic transfer" scenerio. https://www.nature.com/articles/s41591-020-0820-9

Yeah, it could have happened in the lab too.

Now, there is no evidence of recombination and no evidence of a progenitor. The RBD is 100% similar in the 6 critical binding residues to the RBD of GD pangolin and nearly 100% in the rest of the RBD. So, you would have to have a recombination event in the past 20-55 years ago, with an assumed increased mutation rate in the spike region and natural selection up to the present. This means that after the past recombination of RaTG13 with some other CoV, since it is the closet so far, it diverged from this ancestor. One line (SARS-CoV2) went on to evolve the RBD that looks exactly like the GD pangolin showing the difference between it and its closest relative RaTG13 (96.2%)

One paper said this was “coincidental convergent evolution.” Yeah, nature just happened to converge, coincidentally, on the exact same amino acid sequence of an RBD that has optimal binding to ACE2 that is already present in GD pangolin. And the idea that some scientists could be working with CoV RBD chimeras that test binding affinity with ACE2 is just poppycock conspiracy theories. https://academic.oup.com/nsr/advance...waa036/5775463

Neither RaTG13 nor GD pangolin have the polybasic cleavage site but this is only 4 amino acids long and has nothing to do with binding to ACE2. Easily mutated in cell lines or intentionally since they knew from previous studies of the flu virus, that some polybasic cleavage sites evolve in cell lines, and thus might help with the cleavage in CoVs. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC114193/

All your paper does is hope for a progenitor to show up eventually under this scenario and does nothing to answer this coincidental convergence. Your paper ends with this regarding the scenario:

For a precursor virus to acquire both the polybasic cleavage site and mutations in the spike protein suitable for binding to human ACE2, an animal host would probably have to have a high population density (to allow natural selection to proceed efficiently) and an ACE2-encoding gene that is similar to the human ortholog.

Yet they have no evidence of any of this. No progenitor and thus no population density and vice-versa even though bats have these population densities. Interestingly, pangolins can’t be long term reservoirs as they show severe symptoms to CoVs (unlike many bat populations), are a small population size as an endangered species, and are solitary. See: Heinrich, S. et al. The global trafficking of pangolins: A comprehensive summary of seizures and trafficking routes from 2010–2015. Trafficking, (2017).

How this is evidence against a lab origin is beyond me! They may discover all of this but not as of NOW.

Originally Posted by subaru5555

Maybe you should write a paper on your groundbreaking finding; I’m sure all of the “goose-stepping” scientists have come to the same conclusions as you, yet have published findings to the contrary, on purpose.

It's not really a finding it is simply taking their own info and properly looking at it and asking questions. I may be wrong but no one seems to be able to say why. They acknowledge such points if you read it carefully and many times are not so confident in their conclusions. At least I read the damn paper - you cite it and are not even familiar with it.

You had your chance to show where I might be wrong or misrepresented them but no all you have is 'conspiracy' - WEAK!

[AfriqueNY]

Originally Posted by Pinta loca

No, he won’t release anything because it’s all made up.

It wouldn’t be the first time this administration lies. We are used to it. We know how this story will end. We also know his supporters will make apologies when nothing gets released.

It’s Groundhog Day. More lies, more excuses...

He is going to release his evidence that Obamas birth certificate was fake any day now. He has people down in Kenya working on it.

[subaru5555]

Originally Posted by Shiloh1

It's not really a finding it is simply taking their own info and properly looking at it and asking questions. I may be wrong but no one seems to be able to say why. They acknowledge such points if you read it carefully and many times are not so confident in their conclusions. At least I read the damn paper - you cite it and are not even familiar with it.

You had you chance to show where I might be wrong or misrepresented them but no all you have is 'conspiracy' - WEAK!

I read the paper, and laughed when you copy-and-pasted part of a sentence as if it were your own words - but forgot to remove the “Fig 1B.” Btw - you also added “not” in front “unique”; the real excerpt actually was “O-linked glycans are unique to SARS-CoV-2“.

And yes, your argument still amounts to conspiracy.

Originally Posted by subaru5555

I read the paper, and laughed when you copy-and-pasted a sentence as if it were your own words - but forgot to remove the “Fig 1B.” Btw - you also added “not” in front “unique”; the real excerpt actually was “are unique to SARS-CoV-2“.

I did no such thing! Demonstrate it! I did not forget to remove the Fig.1b I put it there to show you that their own fig. demonstrates that the O-linked glycans are not predicted by the insertion. You did not even realize that the Fig1b was in your own paper -freaking brilliant!

Thus they (the O-linked glycans) are NOT UNIQUE as they claimed. Do you always F-up when trying to read and comprehend something?

And yes, your argument still amounts to conspiracy.

Nothing but hot air again from the Goose Stepper! Let's see if you can actually articulate what conspiracy I'm offering without misrepresentation, lying, or misdirection?

Next:

This is the “Natural selection in humans following zoonotic transfer” in your cited paper.

This is similar to the above only that it jumped to humans 20-55 years ago, after the recombination event, and then mutated in humans without any symptoms until 2019 when it became what we know as SARS-CoV2 with an exact RBD like GD pangolin. Again, no evidence of this and no progenitor or recombination event. The common ancestor for this virus, and its different varieties (at least 103 and counting – all 99.9+% similar) that developed from it must be in late 2019, as your cited paper says. Yet the closest so far is RaTG13 which, at 96.2%, cannot be the progenitor or most recent common ancestor. Remember SARS and MERS had progenitors of 99.8% and 99.9%.

In this scenario the virus that jumped into humans had the RBD (a recombination event with RaTG13 and GD pangolin) and the subsequently developed the poly cleavage site during the human to human transmission. The RaTG13 diverged and mutated to the 96.2% similarity. But the recombination event would have to happen 20-55 years ago. Why was no one getting sick back then with this high affinity RBD? And how did the RBD not mutate in the 20-55 years? So, the only mutation was the 4 amino acid chain insertion in the polybasic cleavage site and the 3.8% difference with RaTG13. The RBD is one of the most highly mutative regions yet it did not change in 20-55 years when it jumped into humans? I guess it is all possible but so the hell is a lab derived virus that had mutations in cell lines.

The paper says that repeated jumping events might have occurred, like SARS and MERS, but that matters not. These repeated jumps produce single infections and short transmissions that resolve with “no adaptation.” So, for 20-50 years where were these single infections? And why no adaptation in a region that is highly mutative?

This is why the paper calls it “cryptic transmission.” Ok, so now we have cryptic transmission and coincidental convergent evolution but we can never have on the table a lab derived virus – nope that is just poppycock nonsense. Yes, it is possible that this type of transmission takes place but it is hidden and thus there is no evidence of such transmission. But the lab derived virus is also possible. In every study I have seen in cryptic transmission there is adaptation and mutation. Thus, the paper again hopes that in the future serological studies on banked human samples might resolves this. I thought this was already ‘clear’ that it could not be lab derived based upon these points. Yeah sure!

So, no evidence as of yet!

[subaru5555]

Originally Posted by Shiloh1

I did no such thing! Demonstrate it! I did not forget to remove the Fig.1b I put it there to show you that their own fig. demonstrates that the O-linked glycans are not predicted by the insertion.

Thus they (the O-linked glycans) are NOT UNIQUE as they claimed. Do you always F-up when trying to read and comprehend something?


Nothing but hot air again form the Goose Stepper! Let's see if you can actually articulate what conspiracy I'm offering without misrepresentation, lying, or misdirection?

Hahahaha.

If I’m a “goose stepper” for not believing in an absurd conspiracy, so be it.

Originally Posted by subaru5555

Hahahaha.

If I’m a “goose stepper” for not believing in an absurd conspiracy, so be it.

Do you not understand? If so ask questions or make you case. You look so foolish! Come demonstrate you claim that I forgot to remove it? You are goose stepper for blindly believing an authority without even knowing why. Foolish!

Nice edit!

Here is what I posted none of which is copied.

Well looks like it went silent all of a sudden. Oh well, onto the second "notable feature" - the polybasic furin cleavage site and O-linked glycans.

The O-linked glycans are not unique to SARS-CoV2, as is seen in their own Fig.1b. Both Pangolin and RaTG13 have all three. They are thus not a prediction of the proline in the PRRA insertion.

Your paper claimed they were unique and their own fig.1b demonstrates that they are not. Duh!

Moving on:

I don’t think many people are saying it was ‘necessarily’ lab engineered just that it is possible and not a BS conspiracy theory and that it should be looked at more carefully. But many have said that it is necessarily not lab derived – that is BS based upon what we know right now.

Now regarding the “Selection during passage” section where they try to dismiss a lab scenario.

First, they admit that research on SARS-CoV like viruses has been going on for years and they admit that escapes have occurred of SARS-CoV. Second, they admit that it is possible that SARS-CoV2 acquired mutations for the RBD in cell lines. But then they say that because SARS-CoV2 has identical RBG as that of GD pangolin it is more parsimonious that it acquired it via recombination or mutation. But there is no evidence of recombination, no progenitor, and no lines prior to 2019 that show these mutations.

What they don’t consider is the chimeras that have already been done where they use a CoV RBD with a backbone of another virus. That is just as possible. And frankly, at this point, more likely given the points I mention above.

They then try to use the poly basic cleavage site as something meaningful to their position. But the points made above about this region (only 4 amino acids long) is irrelevant particularly given that the O-linked glycans are not unique to SARS-CoV2 since both pangolin and RaTG13 have all three (see their own Fig.1b) – thus these are not predicted by the tropism of the proline. And even if they were mutation in cells lines of these 4 amino acid chains is completely possible given that mutation takes place in cell lines and that other viruses have prolines in the cleavage site. It’s not unique or improbable via mutation lab or otherwise.

Then they have the gall to complain that if this virus was as result of cell lines (which is only one way the other being a chimera which they don’t deal with) it would have had a prior progenitor with genetic similarity. Yet they don’t have one either for their scenarios. But given that there was such secrecy by the CCP and that they destroyed viruses after the outbreak I guess we will never know. But the Chimera scenario is more likely to be the lab derived version not one where cell lines had to develop the RBD – they simple borrowed it from GD pangolin and used the RaTG13 as backbone and then when running cell lines, the poly cleavage site developed its 4 amino acid chain. As noted by this paper they have been working with CoVs for a long time. Both RaTG13 and Pangolin are not native to the area but they were in their labs.

Finally, you don’t need an immune system for the O-linked glycans to develop since they are already present in GD pangolin and RaTG13 as seen in Fig.1b. But even if they were not other methods are available to act like an immune response in the lab.

Then in their conclusion they say: “Although the evidence shows that SARS-CoV-2 is not a purposefully manipulated virus, [have to disagree there] it is currently impossible to prove or disprove the other theories of its origin described here. However, since we observed all notable SARS-CoV-2 features, including the optimized RBD and polybasic cleavage site, in related coronaviruses in nature, we do not believe that any type of laboratory-based scenario is plausible.”

Well, I have disagreed and believe they are wrong about the plausibility given the problems and unanswered questions and lack of evidence regarding their own scenarios.

Then they say that more scientific data could swing it either way – well then, I guess it is not settled after all. Just as this paper also pointed out:

“Many hypotheses involving recombination, convergence and adaptation have been put forward to suggest a probable evolutionary pathway for SARS-CoV-2, but none is supported by direct evidence. The jury is still out as to what animals might serve as reservoir and intermediate hosts of SARS-CoV-2.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7074995/

And this paper: “Direct contact with intermediate host animals or consumption of wild animals was suspected to be the main route of SARS-CoV-2 transmission. However, the source(s) and transmission routine(s) of SARS-CoV-2 remain elusive.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7068984/

Looks like someone has left the house. Hot air goose steppers everywhere