Brufsky & Ambati: "MSH3 Homology and Potential Recombination Link to SARS-CoV-2 Furin Cleavage Site"; potent paper that further thickens the plot with Bruttell & Washburne's endonuclease

"The presence of the 19-nucleotide long RNA sequence including the FCS with 100% identity to the reverse complement of the MSH3 mRNA is highly unusual"

SOURCE:

https://www.frontiersin.org/articles/10.3389/fviro.2022.834808/full

“Among numerous point mutation differences between the SARS-CoV-2 and the bat RaTG13 coronavirus, only the 12-nucleotide furin cleavage site (FCS) exceeds 3 nucleotides.”

Brufsky & Ambati get to the motherload with FIGURE 1: The origin of the furin sequence in SARS-CoV-2. Comparison of the protein sequences at the S1/S2 junction in SARS-CoV, RaTG13, and SARS-CoV-2 demonstrating the presence of the furin cleavage site (FCS) PRRA only in SARS-CoV-2.”

You can see in Figure 1, the match extends beyond the 12-nucleotide insertion to a 19-nucleotide sequence: 5′-CTACGTGCCCGCCGAGGAG-3′ (nt 2733-2751 of SEQ ID11652)

Brufsky & Ambati report: “A BLAST search revealed that a 19 nucleotide portion of the SARS-CoV-2 genome encompassing the furin cleavage site is a 100% complementary match to a codon-optimized proprietary sequence that is the reverse complement of the human mutS homolog (MSH3). The reverse complement sequence present in SARS-CoV-2 may occur randomly but other possibilities must be considered. Recombination in an intermediate host is an unlikely explanation. Single stranded RNA viruses such as SARS-CoV-2 utilize negative strand RNA templates in infected cells, which might lead through copy choice recombination with a negative sense SARS-CoV-2 RNA to the integration of the MSH3 negative strand, including the FCS, into the viral genome. In any case, the presence of the 19-nucleotide long RNA sequence including the FCS with 100% identity to the reverse complement of the MSH3 mRNA is highly unusual and requires further investigations.”

Prior substack in the lab origin confirmatory analysis: