Abstract

WHO. Coronavirus disease (COVID-19) Weekly Epidemiological Update. Coronavirus disease (COVID-2019) situation reports. https://www.who.int/docs/default-source/coronaviruse/situation-reports/20200824-weekly-epi-update.pdf?sfvrsn=806986d1_4. (2020). Platanias, L. C. Mechanisms of type-I- and type-II-interferon-mediated signalling. Nat. Rev. Immunol. 5, 375–386 (2005). Article CAS Google Scholar Hu, Y. et al. The Severe Acute Respiratory Syndrome Coronavirus nucleocapsid inhibits type I interferon production by interfering with TRIM25-mediated RIG-I Ubiquitination. J. Virol. 91, e02143–16 (2017). PubMed PubMed Central CAS Google Scholar McBride, R., Zyl, M. & Fielding, B. The coronavirus nucleocapsid is a multifunctional protein. Viruses 6, 2991–3018 (2014). Article CAS Google Scholar Mu, J. et al. SARS-CoV-2-encoded nucleocapsid protein acts as a viral suppressor of RNA interference in cells. Sci China Life Sci. 63, 1–4 (2020). Article CAS Google Scholar Download references We thank Dr. Ding Gao and the core facility center of Wuhan Institute of Virology for technical help, and Dr. Xinwen Chen (Wuhan, China) for kindly providing materials. This work was supported by the Strategic Priority Research Program of CAS (XDB29010300 to X.Z.), the National Science and Technology Major Project (2018ZX10101004 to X.Z.), the National Natural Science Foundation of China (31800140 to J.M., 81873964 to Y.Q., and 31670161 and 31970169 to X.Z.), the CAS Youth Innovation Promotion Association (2020332 to Y.Q.), the Newton Advanced Fellowship from the Academy of Medical Sciences, UK (NAF005\1002 to X.Z.), the Yunde Hou Academician Fund from National Institute for Viral Disease Control and Prevention (2019HYDQNJJ10 to J.M.), and the China Postdoctoral Science Foundation (2020T130021ZX to Q.Y., 2020M672452 to T.S.). State Key Laboratory of Virology, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences (CAS), Wuhan, Hubei 430071, China Jingfang Mu, Yaohui Fang, Qi Yang, Ting Shu, An Wang, Muhan Huang, Fei Deng, Yang Qiu & Xi Zhou Joint Laboratory of Infectious Diseases and Health, Wuhan Institute of Virology & Wuhan Jinyintan Hospital, CAS, Wuhan, Hubei 430023, China Jingfang Mu, Ting Shu, Muhan Huang, Fei Deng, Yang Qiu & Xi Zhou The University of Chinese Academy of Sciences, Beijing 100049, China An Wang & Xi Zhou Institute of Microbiology, Jiangxi Academy of Sciences, Nanchang, Jiangxi 330029, China Liang Jin & Xi Zhou You can also search for this author in PubMed Google Scholar You can also search for this author in PubMed Google Scholar You can also search for this author in PubMed Google Scholar You can also search for this author in PubMed Google Scholar You can also search for this author in PubMed Google Scholar You can also search for this author in PubMed Google Scholar You can also search for this author in PubMed Google Scholar You can also search for this author in PubMed Google Scholar You can also search for this author in PubMed Google Scholar You can also search for this author in PubMed Google Scholar J.M. performed the experiments with the help of Y.F., Q.Y., T.S., A.W., M.H., L.J., and F.D., J.M., Y.Q. and X.Z. designed the experiments. J.M., Y.Q, and X.Z. interpreted the results and wrote the manuscript. Correspondence to Yang Qiu or Xi Zhou. The authors declare that they have no conflict of interest. Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. Reprints and Permissions Mu, J., Fang, Y., Yang, Q. et al. SARS-CoV-2 N protein antagonizes type I interferon signaling by suppressing phosphorylation and nuclear translocation of STAT1 and STAT2. Cell Discov 6, 65 (2020). https://doi.org/10.1038/s41421-020-00208-3 Download citation Received: 16 June 2020 Accepted: 26 August 2020 Published: 15 September 2020 DOI: https://doi.org/10.1038/s41421-020-00208-3

Highlights

  • 2019) has spread rapidly across the globe since late 2019 and has become a pandemic[1]

  • We found that ectopic expression of N protein significantly inhibited the activation of IFN-stimulated response element (ISRE) activation induced by Sendai virus (SeV) infection (Fig. 1a), and real-time quantitative PCR analysis showed that SeV-induced expressions of ISG56, ISG54, and ISG15 were significantly inhibited in the presence of N protein (Fig. 1b and Supplementary Fig. S1a, b)

  • These results indicate that SARS-CoV-2 N protein can inhibit the phosphorylation of STAT1 and STAT2 induced by SeV infection

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Summary

Introduction

2019) has spread rapidly across the globe since late 2019 and has become a pandemic[1]. We sought to explore whether SARS-CoV-2 N protein suppresses IFN signaling by examining the effect of N protein on Sendai virus (SeV)-induced ISRE-promoter activation via the luciferase reporter assay. Our further results showed that SARS-CoV-2 N protein exhibited a significant inhibitory effect on ISRE-promoter activation induced by either IFN-2α or IFN-β (Fig. 1c, d), indicating that SARS-CoV-2 N protein can act as an antagonist of IFN signaling.

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