One thing I did not realize is that US researchers who conducted gain of function research tried to downplay and discredit the possibility of the virus originating from the wuhan lab. There was an anti-lab theory Lancet statement signed by scientists, and "Daszak had not only signed but organized the influential Lancet statement, with the intention of concealing his role and creating the impression of scientific unanimity."
Plus there's all the stuff about the miners shoveling bat poop for weeks and then dying of coronaviruses, and the Wuhan institute collecting and doing gain of function research on these similar-to-SARS samples. And then several of the lab's gain of function researchers became ill in late 2019. And there's the weird renaming of samples to hide the unmatched closeness of the mine samples and covid. This is just the absolute surface of the article. There's too much to list here
Edit: here's another amazement for the list: "Shi Zhengli herself had publicly acknowledged that, until the pandemic, all of her team’s coronavirus research — some involving live SARS-like viruses — had been conducted in less secure BSL-3 and even BSL-2 laboratories." And the article says "BSL-2 [is] roughly as secure as an American dentist’s office."
I can’t find sources for this right now but apparently Dr Anthony Fauci played a key role in getting the ban lifted. He’s also the head of the NIAID ( https://en.m.wikipedia.org/wiki/Anthony_Fauci ) which (apparently) is the ultimate source for all funding on gain of function research.
So the lead guy we’ve been listening to (and still are) for scientific advice on this pandemic is entangled in a massive conflict of interest.
Edit: I assume this is getting down-voted either because is sounds like conspiracy theory or just everyone has already heard it and it's not news. Fauci has already admitted having been involved in funding Wuhan - https://nypost.com/2021/05/25/fauci-admits-nih-funding-of-wu... - that on it's own should not have been something he first admitted to in May 2021, while holding such a responsible position. Looking for more sources right now...
Edit 2: In this article from December 2011 - https://www.washingtonpost.com/opinions/a-flu-virus-risk-wor... - you have Fauci making the case for creating viruses in a lab;
> "Given these uncertainties, important information and insights can come from generating a potentially dangerous virus in the laboratory."
It doesn't explicitly mention gain of function but - while raising the concerns, it's arguing for research which would include gain of function. Meanwhile listening to this panel discussion which included Fauci from Nov 2017 - https://www.c-span.org/video/?437187-1/johns-hopkins-forum-e... ... again he's arguing for more aggressive types of research
Whether or not anything shady was happening, the conflict of interest is clear.
The “engineered” component is about the Furin cleavage site on the sars-cov-2 spike protein.
The virus shares 92% genetic similarity to bat coronaviruses, except the spike protein, which is nearly identical to a pangolin coronavirus(which is otherwise only ~38% similar) with one key exception: The Furin cleavage site using “lab standard” sequences.
The gene sequence for the amino acids in the furin site in CoV-2 uses a very rare set of two codons, three letter words so six letters in a row, that are rarely used individually and have never been seen together in tandem in any coronaviruses in nature. But these same ‘rare in nature’ codons turn out to be the very ones that are always used by scientists in the laboratory when researchers want to add the amino acid arginine, the ones that are found in the furin site. When scientists add a dimer of arginine codons to a coronavirus, they invariably use the word, CGG-CGG, but coronaviruses in nature rarely (<1%) use this codon pair. For example, in the 580,000 codons of 58 Sarbecoviruses the only CGG pair is CoV-2; none of the other 57 sarbecoviruses have such a pair.According to Andersen, the CGG codon isn't quite as rare in coronaviruses. He also comments that the stability of the CGG codon in the Furin cleavage site has been remarkably high over the course of the pandemic, which is a hint that the CGG codon may be selected for and crucial for the virus.
Quoting him:
> Now, the codons. Here, Baltimore is talking about the two codons coding for the first two arginines (R) following the P - CGG. The CGG codon is rare in viruses because it's an example of an unmethylated "CpG" site that can be bound by TLR9, leading to immune cell activation.
> Despite being rare, however, CGG codons are found in all coronaviruses, albeit at low frequency. Specifically, of all arginine codons, CGG is used at these frequencies in these viruses:
> SARS: 5% SARS2: 3% SARSr: 2% ccCoVs: 4% HKU9: 7% FCoV: 2%
> Nothing unusual here.
> Furthermore, if we go back to the FCoV sequences and compare them to SARS-CoV-2 at the nucleotide level you'll see that FCoV also uses CGG to code for R immediately following the P. The next R is CGA (non-CpG) in FCoV, while it's CGG in SARS-CoV-2 - one nucleotide difference.
> We see CGG multiple times in different ways - here's an example comparing another "PR" stretch between SARS-CoV-2, RaTG13, and SARS-CoV in the N gene. Note how SARS-CoV-2 and RaTG13 both use CGG, while SARS-CoV-2 uses CGC for the first R, while later R's are coded by CGT or AGA
> One final point about the CGG codons in the FCS - if they were somehow "unnatural", we'd see SARS-CoV-2 evolve away from "CGG" during the ongoing pandemic. We have more than a million genomes to analyze, so what do we find if we look at synonymous mutations at the "CGG_CGG" site?
> Remarkably stable. Specifically, CGG is 99.87% conserved in the first codon and 99.84% conserved in the second.
> This is very strong evidence that SARS-CoV-2 'prefers' CGG in these positions.