Johnson and Menachery et al.: "Furin Cleavage Site Is Key to SARS-CoV-2 Pathogenesis"; there is a critical role for the furin cleavage site (PRRA) insertion in SARS-CoV-2 replication & pathogenesis.
Loss of furin cleavage site attenuates (weakens) COVID pathogenesis; reason I posted is to remind that the chance of this furin cleavage site being inserted into COVID virus via evolution is near 0.
All evidence today says this is man-made deliberate made.
SOURCE 1:
https://pubmed.ncbi.nlm.nih.gov/32869021/
‘SARS-CoV-2 has resulted in a global pandemic and shutdown economies around the world. Sequence analysis indicates that the novel coronavirus (CoV) has an insertion of a furin cleavage site (PRRAR) in its spike protein. Absent in other group 2B CoVs, the insertion may be a key factor in the replication and virulence of SARS-CoV-2. To explore this question, we generated a SARS-CoV-2 mutant lacking the furin cleavage site (ΔPRRA) in the spike protein. This mutant virus replicated with faster kinetics and improved fitness in Vero E6 cells. The mutant virus also had reduced spike protein processing as compared to wild-type SARS-CoV-2. In contrast, the ΔPRRA had reduced replication in Calu3 cells, a human respiratory cell line, and had attenuated disease in a hamster pathogenesis model.
Despite the reduced disease, the ΔPRRA mutant offered robust protection from SARS-CoV-2 rechallenge. Importantly, plaque reduction neutralization tests (PRNT 50 ) with COVID-19 patient sera and monoclonal antibodies against the receptor-binding domain found a shift, with the mutant virus resulting in consistently reduced PRNT 50 titers.
Together, these results demonstrate a critical role for the furin cleavage site insertion in SARS-CoV-2 replication and pathogenesis. In addition, these findings illustrate the importance of this insertion in evaluating neutralization and other downstream SARS-CoV-2 assays.’
SOURCE 2:
https://pubmed.ncbi.nlm.nih.gov/33494095/
‘Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-a new coronavirus that has led to a worldwide pandemic1-has a furin cleavage site (PRRAR) in its spike protein that is absent in other group-2B coronaviruses2. To explore whether the furin cleavage site contributes to infection and pathogenesis in this virus, we generated a mutant SARS-CoV-2 that lacks the furin cleavage site (ΔPRRA).
Here we report that replicates of ΔPRRA SARS-CoV-2 had faster kinetics, improved fitness in Vero E6 cells and reduced spike protein processing, as compared to parental SARS-CoV-2. However, the ΔPRRA mutant had reduced replication in a human respiratory cell line and was attenuated in both hamster and K18-hACE2 transgenic mouse models of SARS-CoV-2 pathogenesis. Despite reduced disease, the ΔPRRA mutant conferred protection against rechallenge with the parental SARS-CoV-2.
Importantly, the neutralization values of sera from patients with coronavirus disease 2019 (COVID-19) and monoclonal antibodies against the receptor-binding domain of SARS-CoV-2 were lower against the ΔPRRA mutant than against parental SARS-CoV-2, probably owing to an increased ratio of particles to plaque-forming units in infections with the former. Together, our results demonstrate a critical role for the furin cleavage site in infection with SARS-CoV-2 and highlight the importance of this site for evaluating the neutralization activities of antibodies.’
the opening sentence of this study is incorrect. the virus DID NOT result in the shutting down of economies world wide. that fault lies with our incredibly STUPID leaders who somehow thought that staying inside could stop a respiratory virus. never could, never would, never again
I was furiously reading everything I could get my hands on in fairly early 2020, and I remember reading a detailed article about the furin cleavage site in this virus and how it would only get there as a result of lab manipulation, it would not occur in nature. I wish I'd kept the article, but at the time, I didn't know the importance of all I was reading and how it would play out later.