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SARS-CoV-2 Nsp15 antagonizes the cGAS-STING-mediated antiviral innate immune responses.

Hsin-Ping ChiuYao-Yu YeoTsoi Ying LaiChuan-Tien HungShreyas KowdleGriffin D HaasSizun J JiangWeina SunBenhur Lee
Published in: bioRxiv : the preprint server for biology (2024)
Host innate immune system serves as the primary defense against pathogens, including SARS-CoV-2. Co-evolving with the hosts, viruses develop multiple approaches to escape the host surveillance. SARS-CoV-2 silences and dysregulates innate immune responses, and the chaos of antiviral IFN responses highly correlates to COVID-19 disease severity. Nsp15 is a conventional innate immune antagonist across coronaviruses, but the biological impact about SARS-CoV-2 Nsp15 is still unclear. Here, we provide a novel insight that SARS-CoV-2 Nsp15 hampers the expression of innate immune regulator - cGAS and STING via its endoribonuclease activity, then further ameliorates virus replication.
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