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To dive deeper down the rabbit hole, I read WIV's 2017 paper on their coronavirus research that the cables reference. https://journals.plos.org/plospathogens/article?id=10.1371/j... TL;DR they constructed chimeras from multiple versions of bat coronaviruses to create different variations in the "receptor binding domain," specifically the genes encoding the spike protein and ORF8a. They also analyze ORF8b and ORF3b sequences, specifically noting versions of ORF3b they've studied can "antagonize interferon function" (interferons boost immune system response) and discussing their own previous studies on ORF3b. The aim of the chimeras is to create a virus targeting the human ACE2 receptor like SARS-CoV did. They succeed — noting that some of their variants "have a stronger effect than SARS-CoV" — and also note "It is very interesting to investigate in further studies whether [one wild virus variant's] ORF3b and other versions of truncated ORF3b such as [their chimeric virus variants] also show [interferon] antagonism profiles."

Reading a paper from NIH on COVID-19 sequencing — https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7180649/ — guess what gets implicated?

"The SARS-CoV-2 genome was reported to possess 14 ORFs encoding 27 proteins ... When researchers compare the SARS-CoV-2 with the SARS-CoV at the amino acid level, they found the SARS-CoV-2 was quite similar to the SARS-CoV, but there were some notable differences in the 8a, 8b, and 3b protein. [Emphasis mine.]"

I don't know a lot about this subject. But as a layperson, it seems a little suspicious that WIV was making SARS-like coronaviruses in Wuhan, where the outbreak started, from bat viruses collected from Yunan, where the closest living relative of COVID-19 is from, and experimenting specifically with the proteins that are the most-novel in COVID-19 as compared to SARS?



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