Journal
CELL DISCOVERY
Volume 7, Issue 1, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/s41421-021-00275-0
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Funding
- National Key R&D Program of China [2020YFC0841000]
- Strategic Priority Research Program of Chinese Academy of Sciences [XDB29010302]
- National Natural Science Foundation of China [31800732]
- Key Research Programs of Frontier Sciences - Chinese Academy of Sciences
- Chinese Academy of Sciences
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The SARS-CoV-2 nucleocapsid protein impairs stress granule formation induced by viral RNA, promoting viral replication. Deficiency of PKR or G3BP1 disrupts antiviral stress granule formation and enhances SARS-CoV-2 replication.
The newly emerging coronavirus SARS-CoV-2 causes severe lung disease and substantial mortality. How the virus evades host defense for efficient replication is not fully understood. In this report, we found that the SARS-CoV-2 nucleocapsid protein (NP) impaired stress granule (SG) formation induced by viral RNA. SARS-CoV-2 NP associated with the protein kinase PKR after dsRNA stimulation. SARS-CoV-2 NP did not affect dsRNA-induced PKR oligomerization, but impaired dsRNA-induced PKR phosphorylation (a hallmark of its activation) as well as SG formation. SARS-CoV-2 NP also targeted the SG-nucleating protein G3BP1 and impaired G3BP1-mediated SG formation. Deficiency of PKR or G3BP1 impaired dsRNA-triggered SG formation and increased SARS-CoV-2 replication. The NP of SARS-CoV also targeted both PKR and G3BP1 to impair dsRNA-induced SG formation, whereas the NP of MERS-CoV targeted PKR, but not G3BP1 for the impairment. Our findings suggest that SARS-CoV-2 NP promotes viral replication by impairing formation of antiviral SGs, and reveal a conserved mechanism on evasion of host antiviral responses by highly pathogenic human betacoronaviruses.
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