SARS-CoV-2 and human cold coronavirus OC43 inhibit stress granule formation through Nsp15 protein

By Dr. Chinta SidharthanDec 21 2022Reviewed by Aimee Molineux In a recent study published in the journal PLOS Pathogens, researchers investigated the mechanisms through which the human common cold Betacoronavirus OC43 and severe acute respiratory syndrome coronavirus 2 inhibit the formation of stress granules.

Understanding how viruses like SARS-CoV-2 inhibit the formation of stress granules could provide therapeutic targets to improve cellular resistance to infections. Additionally, the analyses were repeated using immunofluorescence staining with other stress granule markers such as Ras-guanosine triphosphate ase-activating protein SH3-domain-binding proteins 1 and 2 , and T-cell internal antigen 1 , as well as eukaryotic translation initiation factors 4 subunit G and 3 subunit B , to determine whether the inhibition of stress granule formation by HCoV-OC43 was limited to stress granules containing TIAR.

Results The results reported no stress granule formation in cells infected with HCoV-OC43 and SARS-CoV-2. Both coronaviruses also inhibited eIF2α phosphorylation and stress granule formation from exogenous stress. Nucleocapsid protein and Nsp15 from HCoV-OC43 and SARS-CoV-2 inhibited stress granule formation when overexpressed ectopically. Additionally, the Nsp15 protein from HCoV-OC43 and SARS-CoV-2 also inhibited the eIF2α phosphorylation induced by sodium arsenite.

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