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Activation and evasion of type I interferon responses by SARS-CoV-2 #MMPMID32733001
Lei X; Dong X; Ma R; Wang W; Xiao X; Tian Z; Wang C; Wang Y; Li L; Ren L; Guo F; Zhao Z; Zhou Z; Xiang Z; Wang J
Nat Commun 2020[Jul]; 11 (1): 3810 PMID32733001show ga
The pandemic of COVID-19 has posed an unprecedented threat to global public health. However, the interplay between the viral pathogen of COVID-19, SARS-CoV-2, and host innate immunity is poorly understood. Here we show that SARS-CoV-2 induces overt but delayed type-I interferon (IFN) responses. By screening 23 viral proteins, we find that SARS-CoV-2 NSP1, NSP3, NSP12, NSP13, NSP14, ORF3, ORF6 and M protein inhibit Sendai virus-induced IFN-beta promoter activation, whereas NSP2 and S protein exert opposite effects. Further analyses suggest that ORF6 inhibits both type I IFN production and downstream signaling, and that the C-terminus region of ORF6 is critical for its antagonistic effect. Finally, we find that IFN-beta treatment effectively blocks SARS-CoV-2 replication. In summary, our study shows that SARS-CoV-2 perturbs host innate immune response via both its structural and nonstructural proteins, and thus provides insights into the pathogenesis of SARS-CoV-2.
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Nat+Commun 2020 ; 11 (1): 3810
