You've got me wrong. I'm not talking about weaponization. Labs are actively creating these very types of mutations out of scientific curiosity. Sometimes it's by forced mutation: https://www.sciencedirect.com/science/article/pii/S0042682212004187 Sometimes it's by direct engineering: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2738192/ https://www.ncbi.nlm.nih.gov/pubmed/26545254 https://www.ncbi.nlm.nih.gov/pubmed/30310104 Scientists are taking these very viruses and mutating them to better understand their functions, including cross-species infection. I am simply wondering if someone goofed when doing something we know is being done.To study the mechanisms underlying the host cell specificity and susceptibility to coronavirus and coronavirus–host interactions, the Beaudette strain of IBV was adapted from chicken embryo to a monkey kidney cell line, Vero, by continuous propagation for 65 passages (Shen et al., 2003, Shen et al., 2004).
Site-directed mutagenesis studies revealed that the S1/S2 cleavage by furin was not necessary for, but could promote, syncytium formation by and infectivity of IBV in Vero cells. In contrast, the second site is involved in the furin dependence of viral entry and syncytium formation. Mutations of the second site from furin-cleavable RRRR/S to non-furin-cleavable PRRRS and AAARS, respectively, abrogated the furin dependence of IBV entry.
Using a molecular cDNA infectious clone to generate a corresponding recombinant virus, we show for the first time that such point mutation in the HCoV-OC43 S glycoprotein creates a functional cleavage site between the S1 and S2 portions of the S protein. While the corresponding recombinant virus retained its neuroinvasive properties, this mutation led to decreased neurovirulence while potentially modifying the mode of virus spread, likely leading to a limited dissemination within the CNS.
Here we engineered full, partially deleted (-29 nt), and fully deleted ORF8 into a SARS-CoV infectious cDNA clone, strain Frankfurt-1. Replication of the resulting viruses was compared in primate cell cultures as well as Rhinolophus bat cells made permissive for SARS-CoV replication by lentiviral transduction of the human angiotensin-converting enzyme 2 receptor.