Document Type
Article
Publication Date
2022
Keywords
Sars-cov-2 Spike, Furin Cleavage Site, MSH3 Gene, Sequence Homology, Recombinability
Digital Object Identifier (DOI)
https://doi.org/10.3389/fviro.2022.834808
Abstract
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. 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.
Rights Information
This work is licensed under a Creative Commons Attribution 4.0 License.
Was this content written or created while at USF?
Yes
Citation / Publisher Attribution
Frontiers in Virology, v. 2, art. 834808
Scholar Commons Citation
Ambati, Balamurali K.; Varshney, Akhil; Lundstrom, Kenneth; Palù, Giorgio; Uhal, Bruce D.; Uversky, Vladimir N.; and Brufsky, Adam M., "MSH3 Homology and Potential Recombination Link to SARS-CoV-2 Furin Cleavage Site" (2022). Molecular Medicine Faculty Publications. 931.
https://digitalcommons.usf.edu/mme_facpub/931
