As for furin (translated):
2020:
Although the above analyzes suggest that SARS-CoV-2 might bind to human ACE2 with high affinity, computational analyzes predict that the interaction is not ideal and that the RBD sequence is different from those presented in SARS-CoV as being optimal for receptor binding. Thus, high affinity binding of the SARS-CoV-2 spike protein to human ACE2 is most likely the result of natural selection on human or human-like ACE2 that allows for another optimal binding solution to arise. This is strong evidence that SARS-CoV-2 is not the product of deliberate manipulation.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7095063/In 2021:
A four amino acid insertion in the SARS-CoV-2 spike protein occurred during its emergence from an animal reservoir and created a suboptimal furin CS. Here we propose a mechanism by which this confers an advantage to the virus in the human respiratory tract, enabling efficient human-to-human transmission....
..... The presence of a CS furin at the S1/S2 junction is not uncommon in human coronaviruses; while half of human seasonal coronaviruses as well as MERS-CoV contain furin CSs, the remaining strains and SARS-CoV do not. 6, 16. Thus, furin-induced tip cleavage is not an absolute requirement for efficient human respiratory transmission. Surveillance of animal coronaviruses will likely be important for predicting and preventing future pandemics. We suggest that the gain of furin CS in broader SARS-related coronaviruses is a cause for concern.
https://www.nature.com/articles/s41564- ... 08-w#Sec102022:
The furin cleavage site of SARS-CoV-2 was not changed
Harrison and Sachs' claim that the Sarbecovirus Spike amino acid sequence alignment illustrates "the unusual nature of the [SARS-CoV-2] FCS" is misleading. FCS are common in coronaviruses and present in representatives of four out of five betacoronavirus subgenera. The highly variable nature of the S1/S2 junction is easily seen by inspecting a precise alignment of Sarbecovirus Spikes.
2023:
SARS-CoV-2 has continued to evolve as it spreads through the population, and we have learned more about its pathogenicity and transmission determinants. As previously reported in The Lancet Microbe, one of these determinants is the unusual furin cleavage site (FCS) on its spike protein. 1
Although it has been proposed that the FCS may have been engineered, it is becoming increasingly clear that natural selection is in fact the driving factor in its acquisition and functionality, through recombination and epistasis.
https://www.thelancet.com/journals/lanmic/article/PIIS2666-5247(23)00144-1/fulltextMadame Chan wants to sell her book (which was published in 2021), and we can understand her.
Alina Chan, biologist at the Broad Institute and Matt Ridley, science journalist (also ex-banker), have just published “Viral”, an investigation into the origins of Sars-CoV-2. They point out the weaknesses of the animal origin thesis, without however dismissing it. Above all, they reconstruct the web of elements which make the hypothesis of an accidental leak from a laboratory plausible. Plausible, but not necessarily true. The story reinforces doubts without providing definitive proof. Ultimately, there remains a much more convincing call for a moratorium on the genetic manipulation of pathogens., which Alina Chan explained to Heidi.news.
https://www.heidi.news/sante/le-livre-q ... aboratoire