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Opinion CIA Now Believes Covid-19 Came From Lab Leak

Every time I hear people talking about Covid's origins I keep thinking of that segment Jon Stewart pointed out the absurdity in not taking the lab leak seriously
It's taken seriously it just isn't proven. If anything it's laymen without expertise in the field claiming it makes so much sense it came from the lab that it must be true.
 
Shocked!

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It's not like virtually every person not in the Left Cult / Democrat figured this out years ago. It's nice for the CIA with all of their capabilities to finally catch up.
 
I honestly don't understand what people don't understand about the "low confidence" caveat. It just means that of the two prevailing theories, they aren't by any means certain but believe the lab leak theory to be the most likely. On the one hand, they wouldn't bet the house on it, but on the other hand, if they were forced to bet, that's the bet they'd make.

No one has high confidence in the origins of Covid. That's not what the outrage is about, and pointing that out isn't a good rebuttal to the outrage. The outrage is about the wet market origin people posturing like they had high confidence in their theory, when they clearly did not, as a justification for taking draconian measures to shut down discussion and stomp out the at least equally likely (more likely, according to the FBI and CIA) lab leak theory.

It's about the authoritarian posturing of it all. And it's both enlightening and disheartening to see people who characterize themselves as principled anti-authoritarians flipping so easily to authoritarian apologetics just because, in a particular moment, it suits their political agendas and leanings.
Gave you the like but what difference does the origin of the virus make in regards to the protocols that were put in place due to it's virulence?
 
It doesn’t. I explained your misconception you just didn’t understand it. Washburne’s (unpublished) paper is a joke and even most lab leakers find it comically unconvincing. It’s a textbook example of selection bias combined with insufficient sampling, which is why he intentionally didn’t adjust for multiple comparisons. I’d fail my students for something so egregious. To demonstrate what everyone else knew, this author extended the same model to a larger set of Betacoronaviruses and big shocker — there’s absolutely nothing special about those restriction sites in sars2. So to answer your question, the odds are pretty high. Well, unless you think all of those viruses in nature are genetically engineered as well.
I am asking you specifically to respond to this: Two BsaI cut sites in Covid-19 are found in the same location as previously mentioned engineered cut sites, published in 2017: https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1006698&type=printable

What are the chances of random recombination events in nature mimicking previously published engineering twice?
 
I am asking you specifically to respond to this: Two BsaI cut sites in Covid-19 are found in the same location as previously mentioned engineered cut sites, published in 2017: https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1006698&type=printable

What are the chances of random recombination events in nature mimicking previously published engineering twice?
Are you asking as a gotcha and have the answer or do you just not know either?
 
I am asking you specifically to respond to this: Two BsaI cut sites in Covid-19 are found in the same location as previously mentioned engineered cut sites, published in 2017: https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1006698&type=printable

What are the chances of random recombination events in nature mimicking previously published engineering twice?
And I replied specifically to that point. Again, you’re just not understanding. I’ll try one last time:

The Washburne/Bruttel paper was using the Hu 2017 paper as its basis for analyzing those specific sites. Even ignoring the flagrant selection bias, it STILL is not an improbable finding when you consider the diversity of coronaviruses and restriction sites. Within a relatively small sample of coronaviruses from nature, DOZENS met the IVGA fingerprint criteria based on locations of the restriction sites and lengths in the Ben Hu paper you JUST CITED. In other words, not improbable.

If you’re unwilling to take the time to learn the science behind the claims you’re making, it’s not worth my effort to respond.
 
Are you asking as a gotcha and have the answer or do you just not know either?
He think it’s highly improbable not because of his understanding of the science, but because he read a paper that’s been rejected by peer review (probably several times now) yet it manages to convince the impressionable lay population.

Even within the lab leak community most have distanced themselves from that argument. It was piss poor reasoning from the beginning.
 
Are you asking as a gotcha and have the answer or do you just not know either?
I am attempting to continue a conversation from the previous thread, which starts with this post from me:
Which virus recombined with which virus to get the furin cleavage site into a SARS virus?
It would save me effort if you had gone back to that thread and reviewed the exchange before posting your question, but I will attempt cliffs for you.

The argument is whether Covid-19 (SARS-CoV-2) is of natural origin (Greco_Wiz's argument) versus lab origin (my argument). SARS-CoV-2 differs from SARS-CoV-1 in that SARS-CoV-2 has a furin cleavage site (FCS) in its genetic blueprint. The natural versus lab origin argument needs to explain how that furin clevage site got there.

The natural origin argument is that a SARS virus (without FCS) got together with another virus (with FCS) and produced SARS-CoV-2 (with FCS). This getting together is called recombination. Viruses are classified by genetic relatedness just like animals, so the question the natural origin argument must answer is: Which virus recombined with which virus to produce SARS-CoV-2? Greco_Wiz cannot answer this question except to acknowledge that the recombination partners would be so unlikely as to constitute a unique in history event, as I have described here:
I'm glad that your article points out the problem of recombination being unlikely between viruses that are not closely related, which is why I asked you to specifically name the viruses that recombined:
The main reason why the short FCS sequence in SARS-CoV-2 (12 nucleotide insertion) has been hotly discussed is because it stood out like a sore thumb in side-by-side sequence comparisons to known coronaviruses in early 2020. (Since then, scientists have found plenty of naturally occurring FCS in the wider CoV sub-family, but not in the sarbecovirus sub-genus specifically)

Just because something is rare or even unique among currently known sarbecovirus members is however not good evidence for artificial introduction given the high sequence diversity at S1/S2 (see below).

Arguing for a "unique" event, to me, does not constitute overwhelming evidence.

Back in the day when DNA evidence from a drop of blood was being used to place OJ Simpson to the murder scene, whole genome sequencing was not as advanced as today, but it was argued that restriction fragment testing was better than fingerprints.
From:
Dr. Robin Cotton, Lab director of Cellmark Diagnostics, testified May 8–15, 1995.[23] She testified to restriction fragment length polymorphism (RFLP) testing, the most precise DNA-matching at the time. She testified that blood found on a sock in Simpson's bedroom was Nicole Brown's with a 1-in-170 million chance of error, and that the blood drops next to bloody footprints near Nicole's body was Simpson's with a 1-in-9.7 billion chance of error

And researchers "found that SARS-CoV has the restriction site fingerprint that is typical for synthetic viruses."
From: https://www.biorxiv.org/content/10.1101/2022.10.18.512756v1
Lay Summary To construct synthetic variants of natural coronaviruses in the lab, researchers often use a method called in vitro genome assembly. This method utilizes special enzymes called restriction enzymes to generate DNA building blocks that then can be “stitched” together in the correct order of the viral genome. To make a virus in the lab, researchers usually engineer the viral genome to add and remove stitching sites, called restriction sites. The ways researchers modify these sites can serve as fingerprints of in vitro genome assembly.

We found that SARS-CoV has the restriction site fingerprint that is typical for synthetic viruses. The synthetic fingerprint of SARS-CoV-2 is anomalous in wild coronaviruses, and common in lab-assembled viruses. The type of mutations (synonymous or silent mutations) that differentiate the restriction sites in SARS-CoV-2 are characteristic of engineering, and the concentration of these silent mutations in the restriction sites is extremely unlikely to have arisen by random evolution. Both the restriction site fingerprint and the pattern of mutations generating them are extremely unlikely in wild coronaviruses and nearly universal in synthetic viruses. Our findings strongly suggest a synthetic origin of SARS-CoV2.

Can we apply Occam's Razor to the probability of a "unique" recombination event to a common lab-assembly event (anomalous in nature)?
Now we come to my argument, of lab origin. There was literally a research proposal called DARPA to insert a furin cleavage site into a bat coronavirus. Alina Chan even got Linfa Wang to credit Ralph Baric (who has worked with Wuhan Institute of Virology’s Shi Zhengli) as being the origin of the FCS proposal.
I regularly check Alina Chan's twitter: https://twitter.com/Ayjchan

In a debate organized by@ScienceMagazine, virologist Linfa Wang is asked by@Ayjchan whose idea it was to insert furin cleavage sites into bat coronaviruses in a rejected DARPA proposal: https://theintercept.com/2021/09/23/coronavirus-research-grant-darpa/

Answer: Univeristy of North Carolina gain of function researcher Ralph Baric


The circumstantial evidence is overwhelming, but can we see the evidence of human tampering in the SARS-CoV-2 genome itself? Genetic manipulation by humans involves cutting up larger genetic sequences into smaller ones, inserting extra genetic sequences, and reassembling into the larger sequence. The cutting is done by restriction enzymes (examples are BsmBI and BsaI that have been used in previous research) at restriction sites on the genetic sequence. Scientists insert extra restriction sites into a genetic sequence to make the cut up fragments more uniform in size. Greco_Wiz will not accept that the even-spacedness alone of BsmBI and BsaI in SARS-CoV-2 is evidence of lab origin because a minority of viruses also have even spacing. But the argument goes beyond just even spacing because two BsaI cut sites in Covid-19 (SARS-CoV-2) are found in the same location as previously mentioned engineered cut sites, published in 2017: https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1006698&type=printable

So now, Greco_Wiz not only needs to account for the FCS in SARS-CoV-2 but also for the two BsaI cut sites, and he will never name specific recombination partners because there aren't any that make sense. But it makes perfect sense that scientists manipulated viral genetic sequences exactly following past published procedures to achieve the exact manipulation proposed: Inserting a furin cleavage site into a bat coronavirus proposed in DARPA, likely by Ralph Baric.
 
S

Do you really think that has nothing to do with Racliffe being put in charge?

I'm sure that pushed it or those involved realized they wanted to keep their jobs before he dealt with it.

But, let's be honest... I think we all believe that's exactly where it came from with pretty solid certainty.
 
I am attempting to continue a conversation from the previous thread, which starts with this post from me:

It would save me effort if you had gone back to that thread and reviewed the exchange before posting your question, but I will attempt cliffs for you.

The argument is whether Covid-19 (SARS-CoV-2) is of natural origin (Greco_Wiz's argument) versus lab origin (my argument). SARS-CoV-2 differs from SARS-CoV-1 in that SARS-CoV-2 has a furin cleavage site (FCS) in its genetic blueprint. The natural versus lab origin argument needs to explain how that furin clevage site got there.

The natural origin argument is that a SARS virus (without FCS) got together with another virus (with FCS) and produced SARS-CoV-2 (with FCS). This getting together is called recombination. Viruses are classified by genetic relatedness just like animals, so the question the natural origin argument must answer is: Which virus recombined with which virus to produce SARS-CoV-2? Greco_Wiz cannot answer this question except to acknowledge that the recombination partners would be so unlikely as to constitute a unique in history event, as I have described here: Now we come to my argument, of lab origin. There was literally a research proposal called DARPA to insert a furin cleavage site into a bat coronavirus. Alina Chan even got Linfa Wang to credit Ralph Baric (who has worked with Wuhan Institute of Virology’s Shi Zhengli) as being the origin of the FCS proposal.The circumstantial evidence is overwhelming, but can we see the evidence of human tampering in the SARS-CoV-2 genome itself? Genetic manipulation by humans involves cutting up larger genetic sequences into smaller ones, inserting extra genetic sequences, and reassembling into the larger sequence. The cutting is done by restriction enzymes (examples are BsmBI and BsaI that have been used in previous research) at restriction sites on the genetic sequence. Scientists insert extra restriction sites into a genetic sequence to make the cut up fragments more uniform in size. Greco_Wiz will not accept that the even-spacedness alone of BsmBI and BsaI in SARS-CoV-2 is evidence of lab origin because a minority of viruses also have even spacing. But the argument goes beyond just even spacing because two BsaI cut sites in Covid-19 (SARS-CoV-2) are found in the same location as previously mentioned engineered cut sites, published in 2017: https://journals.plos.org/plospathogens/article/file?id=10.1371/journal.ppat.1006698&type=printable

So now, Greco_Wiz not only needs to account for the FCS in SARS-CoV-2 but also for the two BsaI cut sites, and he will never name specific recombination partners because there aren't any that make sense. But it makes perfect sense that scientists manipulated viral genetic sequences exactly following past published procedures to achieve the exact manipulation proposed: Inserting a furin cleavage site into a bat coronavirus proposed in DARPA, likely by Ralph Baric.
Wrong on all accounts. I’ve described three times and cited a paper which demonstrates the sites are not particularly unusual.

As for DARPA, you either haven’t read the proposal or don’t understand it. The inserts proposed are at S2 while the FCS in SARS-COV2 is at s1/s2. Entirely different would be an understatement. And the proposal didn’t suggest a 12 nucleotide out of frame insertion (duh!) but guess what, that’s exactly what happens in nature with polymerase slippage. Or did the WIV hire a drunk technician who inserted a non optimal sequence out of frame which was never recommended by any model simulation or paper previously?
 
Wrong on all accounts. I’ve described three times and cited a paper which demonstrates the sites are not particularly unusual.

As for DARPA, you either haven’t read it or don’t understand it. The inserts proposed are at S2 while the FCS in SARS-COV2 is at s1/s2. Entirely different would be an understatement. And the proposal didn’t suggest a 12 nucleotide out of frame insertion (duh!) but guess what, that’s exactly what happens in nature with polymerase slippage. Or did the WIV hire a drunk technician who inserted a non optimal sequence out of frame which was never recommended by any model simulation or paper previously?
If it's exactly what happens in nature then you should have no problem stating which specific virus recombined with which specific virus to get the furin cleavage site into a SARS virus?
 
Neither explanation for the origin would surprise me. It'd be nice to get a definitive answer. Whatever the case it'd be nice to know so we can hopefully take measures to prevent it happening again
 
I'm sure that pushed it or those involved realized they wanted to keep their jobs before he dealt with it.

But, let's be honest... I think we all believe that's exactly where it came from with pretty solid certainty.
I'd say it's probable it either came from the lab or from the market. Where it came from I wouldn't speculate but it's virulence seems hard to deny. It's literally a flu of a hundred years. Luckily our scientific advancements in that time frame have led us into the Space Age and our medical treatments and technology kept the death rate much lower. The main problem we had was too many people being sick at once and there not being enough beds or machines to treat them all at hospitals.
 
If it's exactly what happens in nature then you should have no problem stating which specific virus recombined with which specific virus to get the furin cleavage site into a SARS virus?
Out of curiosity, and I’m really not trying to make you look bad, but what percent of coronaviruses from nature do we estimate we’ve isolated and sequenced?
 
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