Activation and evasion of type I interferon responses by SARS-CoV-2

Xiaobo Lei, Xiaojing Dong, Ruiyi Ma, Wenjing Wang, Xia Xiao, Zhongqin Tian, Conghui Wang, Ying Wang, Li Li, Lili Ren, Fei Guo, Zhendong Zhao, Zhuo Zhou (), Zichun Xiang () and Jianwei Wang ()
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Xiaobo Lei: Chinese Academy of Medical Sciences and Peking Union Medical College
Xiaojing Dong: Chinese Academy of Medical Sciences and Peking Union Medical College
Ruiyi Ma: Chinese Academy of Medical Sciences and Peking Union Medical College
Wenjing Wang: Chinese Academy of Medical Sciences and Peking Union Medical College
Xia Xiao: Chinese Academy of Medical Sciences and Peking Union Medical College
Zhongqin Tian: Chinese Academy of Medical Sciences and Peking Union Medical College
Conghui Wang: Chinese Academy of Medical Sciences and Peking Union Medical College
Ying Wang: Chinese Academy of Medical Sciences and Peking Union Medical College
Li Li: Chinese Academy of Medical Sciences and Peking Union Medical College
Lili Ren: Chinese Academy of Medical Sciences and Peking Union Medical College
Fei Guo: Chinese Academy of Medical Sciences and Peking Union Medical College
Zhendong Zhao: Chinese Academy of Medical Sciences and Peking Union Medical College
Zhuo Zhou: Peking University
Zichun Xiang: Chinese Academy of Medical Sciences and Peking Union Medical College
Jianwei Wang: Chinese Academy of Medical Sciences and Peking Union Medical College

Nature Communications, 2020, vol. 11, issue 1, 1-12

Abstract: Abstract 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-β 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-β 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.

Date: 2020
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DOI: 10.1038/s41467-020-17665-9

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