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SARS-CoV-2 nucleocapsid protein impairs stress granule formation to promote viral replication.
Zheng, Zhou-Qin; Wang, Su-Yun; Xu, Zhi-Sheng; Fu, Yu-Zhi; Wang, Yan-Yi.
  • Zheng ZQ; Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences, Wuhan, Hubei, China.
  • Wang SY; University of Chinese Academy of Sciences, Beijing, China.
  • Xu ZS; Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences, Wuhan, Hubei, China.
  • Fu YZ; Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences, Wuhan, Hubei, China.
  • Wang YY; Key Laboratory of Special Pathogens and Biosafety, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences, Wuhan, Hubei, China. yuzhi.fu@wh.iov.cn.
Cell Discov ; 7(1): 38, 2021 May 25.
Article in English | MEDLINE | ID: covidwho-1243287
ABSTRACT
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.

Full text: Available Collection: International databases Database: MEDLINE Language: English Journal: Cell Discov Year: 2021 Document Type: Article Affiliation country: S41421-021-00275-0

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Full text: Available Collection: International databases Database: MEDLINE Language: English Journal: Cell Discov Year: 2021 Document Type: Article Affiliation country: S41421-021-00275-0