Social GoldenWolf's COVID Vaccine/Lockdown Protest megathread Vol. 2

Excuse my interjection, but what is the overwhelming science explanation for how a Furin cleavage site got naturally into a SARS virus?

The furin sequence is an out of frame insertion and suboptimal in its performance, which is exactly what you’d expect from recombination and the opposite of what would expect to happen with genetic engineering. Not to mention the palindrome sequence just upstream strongly indicates template switching of the polymerase, again exactly what you expect w/ natural recombination. None of this is surprising given the fact that furin sites are found in coronaviruses in nature.
 
The idea that a novel coronavirus didn’t independently originate across the street from a lab in a country with history of leaks that worked on gain of function novel coronaviruses and immediately after that country deleted data, stopped investigations and created a coverup being a kooky conspiracy theory …
Down the street. You mean 10 miles away at market that received relatively little foot traffic, which just happened to be selling mammals susceptible to infection with sars2. Any other Twitter talking points you want to try?
 
Down the street. You mean 10 miles away at market that received relatively little foot traffic, which just happened to be selling mammals susceptible to infection with sars2. Any other Twitter talking points you want to try?
“Twitter talking points”

The idea that you believe that it’s completely coincidental to the point that anyone that believes there is a link between the location of the lab and the location of the outbreak just shows how idiotic you are.

Good day.
 
“Twitter talking points”

The idea that you believe that it’s completely coincidental to the point that anyone that believes there is a link between the location of the lab and the location of the outbreak just shows how idiotic you are.

Good day.
You said down the street, indicating you have no understanding of even the basics of this topic and are regurgitating a talking point you picked up elsewhere.
 
Research?

Its been 5 fkkn years. Why do we have to climb Mount Everest to get a straight answer on this?

Sounds like a cover up. A kindergarten student could sniff out negligence and hijinx over this. Smartsy Fartsy arrogant asshole people like you think you are too smart for your own good.
One side performed thousands of hours of challenging research and published their insights for everyone else. The other side has had an immovable position since day 1 and ignored completely those valuable findings because conspiracy theories are more attractive. Which side is arrogant again?
 
The furin sequence is an out of frame insertion and suboptimal in its performance, which is exactly what you’d expect from recombination and the opposite of what would expect to happen with genetic engineering. Not to mention the palindrome sequence just upstream strongly indicates template switching of the polymerase, again exactly what you expect w/ natural recombination. None of this is surprising given the fact that furin sites are found in coronaviruses in nature.
Which virus recombined with which virus to get the furin cleavage site into a SARS virus?
 
The furin sequence is an out of frame insertion and suboptimal in its performance, which is exactly what you’d expect from recombination and the opposite of what would expect to happen with genetic engineering. Not to mention the palindrome sequence just upstream strongly indicates template switching of the polymerase, again exactly what you expect w/ natural recombination. None of this is surprising given the fact that furin sites are found in coronaviruses in nature.
giphy.gif
 
And we still get this horseshit answer
Which virus recombined with which virus to get the furin cleavage site into a SARS virus?
HKU9 has a near identical furin cleavage sequence.

If you’re actually interested in learning, here’s an excellent article summarizing the literature on why the sars2 genome screams natural.

 
If you’re actually interested in learning, here’s an excellent article summarizing the literature on why the sars2 genome screams natural.

that was very solid. Mainstream media and Big Tech should be amplifying that instead of focusing on the Fauci charade complete with the circus clowns in Washington
 
HKU9 has a near identical furin cleavage sequence.

If you’re actually interested in learning, here’s an excellent article summarizing the literature on why the sars2 genome screams natural.

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)?
 
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)?
Oh look, you found a pre print that was rejected from publication at least once (and at this point probably several times). As I’ve written on this before, I’ll break it down for you.

The authors cherry picked two restriction enzymes out of more than a hundred options, provided no credible justification for why they were chosen and didn’t correct for multiple comparisons. I teach biostats and couldn’t create a better example of p-hacking if I tried.
So what DO their results show? Does SARS-CoV-2 have more cut sites than other CoVs? Nope. Does it have more BsaI and BsmIB sites? Nope. Are the restriction sites in convenient spots for engineering, like the edges of genes or around the RBD or spike gene? Nope. Their own fucking analysis shows that the genome is exactly what you’d expect if it were natural.
Their measure of ‘syntheticness’ is that after cherry picking an enzyme the cut sites are relatively even such that none are more than 8 Kb. This is in a 30kb genome….With 5 such sites. And they think that’s evidence of engineering. But don’t take my word for it. Their own plot literally shows other natural covs have higher ‘syntheticness’ scores using their own metric.
Oh and before this pre print came out, the inferred recombinant ancestral sequence of SARS-CoV- 'recCA' was published. Wow that pattern of restriction sites looks familiar…

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Oh and the authors also conveniently forgot that the silent mutations they think partly implicate engineering do exist in other covs. They’re found in RpYN06.
10435 tgctat gaggcc
11651 ggcctc ttctgt
And it has been shown previously this region is analogous to RpYN06.

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https://www.ncbi.nlm.nih.gov/nuccore/MZ081381.1

Quick tip. Don’t mindlessly cite something because you think it agrees with your position. About that Occam’s razor…

For the rest of your post, I never said the genome alone constitutes overwhelming evidence. I think the genome indicates that SARSCoV2 is unlikely to be genetically engineered. With this evidence alone, it's possible sars2 was a natural virus collected from the wild which subsequently leaked from the lab. I actually think other independent lines of evidence, namely epidemiological and phylogenetic, make the most convincing argument for a zoonotic emergence via wildlife trade.
 
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