windwalker wrote:time for a reviewWhile there is no record of a process of early evolutionary adaptation, SARS-CoV-2′s receptor binding domain (RBD) appears to be highly optimized for binding to human ACE2 (Fig. 2) (Delgrado Blanco et al. 2020; Damas et al. 2020). In this respect, 43% of modelled mutations destabilize the binding energy of the SARS-CoV-2 spike protein RBD to human ACE2, while just 1% of the mutations stabilize it (Delgrado Blanco et al. 2020).Overall, SARS-CoV-2 was remarkably well adapted to humans from its first appearance, yet poorly adapted to bat infection, the natural reservoirs for SARS-r-CoVs, with little evidence for gaining its human adaptation through natural recombination.In summary, the FCS confers SARS-CoV-2 enhanced human pathogenicity and has never been identified in another Sarbecovirus. At the same time, FCSs have been routinely inserted into coronaviruses in gain-of-function experiments, and we provide a hypothesis through which the specific amino acid sequence of SARS-CoV-2′s FCS may have been generated through cell culture.
https://link.springer.com/article/10.10 ... 21-01211-0
No need to review out-of-date and largely retracted or debunked conspiracy theories that have no proof.
We’ve long known that the presence of such a site in SARS-CoV-2 increased its pathogenic power, and we also know that similar features have not been found in any other SARS-like coronavirus (though we may find them in the future). For lab-leak proponents, these facts—combined with certain details of the furin cleavage site’s structure—strongly hint at human intervention. As the science journalist Nicholas Wade argued in an influential lab-leak-theory brief last spring, this genetic insertion “lies at the heart of the puzzle of where the virus came from.” The virologist David Baltimore even told Wade that the structure of the SARS-CoV-2 furin cleavage site was “the smoking gun for the origin of the virus.” (Baltimore later walked back his claim.)
As many scientists have since pointed out, the mere presence of the furin cleavage site is not dispositive of a Frankenstein experiment gone wrong. For example, the same genetic feature has come about, quite naturally and independently, in plenty of other, more distantly related coronaviruses, including those that cause the common cold. According to a “critical review” co-authored by 21 experts on viruses and viral evolution that was posted as a preprint in July, “simple evolutionary mechanisms can readily explain” the site’s presence in SARS-CoV-2, and “there is no logical reason” why it would look the way it does if it had been engineered inside a lab. “Further,” the authors wrote, “there is no evidence of prior research at the [Wuhan Institute of Virology] involving the artificial insertion of complete furin cleavage sites into coronaviruses.”
https://www.theatlantic.com/science/arc ... er/620209/
And:
The article itself, by science writer Nicholas Wade, has become one of the most often-cited pieces in support of the lab-leak hypothesis. The quote from Baltimore is part of its argumentative bedrock.
Here’s the problem: Baltimore regrets using the phrase “smoking gun” to describe his conclusion, and doesn’t agree that it validates the lab-leak theory.
Baltimore told me by email that he made the statement to Wade, also by email, and granted him permission to use it in print. But he added that he “should have softened the phrase ‘smoking gun’ because I don’t believe that it proves the origin of the furin cleavage site but it does sound that way. I believe that the question of whether the sequence was put in naturally or by molecular manipulation is very hard to determine but I wouldn’t rule out either origin.”
Baltimore has made similar statements to others who have asked him about the quote, including Vincent Racaniello of Columbia University, a former lab colleague of Baltimore’s, and Amy Maxmen of Nature. Baltimore told Maxmen that while evolution could have produced the virus, “there are other possibilities and they need careful consideration, which is all I meant to be saying.”
https://www.latimes.com/business/story/ ... eak-theory
And finally:
While the analyses above suggest that SARS-CoV-2 may bind human ACE2 with high affinity, computational analyses predict that the interaction is not ideal7 and that the RBD sequence is different from those shown in SARS-CoV to be optimal for receptor binding7,11. Thus, the high-affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on a human or human-like ACE2 that permits another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of purposeful manipulation.
https://www.nature.com/articles/s41591-020-0820-9