Transmissible Gastroenteritis Virus Papain-Like Protease 1 Antagonizes Production of Interferon- beta through Its Deubiquitinase Activity

文献类型： 外文期刊

第一作者： Hu, Xiaoliang

作者： Hu, Xiaoliang;Kang, Hongtao;Guo, Dongchun;Liu, Jiasen;Liu, Dafei;Jiang, Qian;Li, Zhijie;Qu, Liandong;Qu, Juanjuan

作者机构：

期刊名称：BIOMED RESEARCH INTERNATIONAL （ 影响因子：3.411； 五年影响因子：3.62 ）

ISSN： 2314-6133

年卷期： 2017 年

页码：

收录情况： SCI

摘要： Coronaviruses (CoVs), such as human coronavirus NL63 (HCoV-NL63), severe acute respiratory syndrome CoV (SARS-CoV), murine hepatitis virus (MHV), porcine epidemic diarrhea virus (PEDV), and Middle East Respiratory Syndrome Coronavirus (MERS-CoV), encode papain-like (PL) proteases that inhibit Sendai virus-(SeV-) induced interferon (IFN-beta) production. Recently, the crystal structure of transmissible gastroenteritis virus (TGEV) PL1 has been solved, which was similar to that of SARS-CoV PL2(pro), which may antagonize host innate immunity. However, very little is known about whether TGEV PL1 can antagonize host innate immune response. Here, we presented evidence that TGEV PL1 encoded by the replicase gene could suppress the IFN-beta expression and inhibit the nuclear translocation of interferon regulatory factor 3 (IRF3). The ability to antagonize IFN-beta production was dependent on the intact catalytic activity of PL1. Furthermore, TGEVPL1 exerted deubiquitinase (DUB) activity which strongly inhibited the retinoic acid-induced gene I-(RIG-1-) and stimulator of interferon gene-(STING-) dependent IFN expression. Our data collectively suggest that TGEV PL1 can inhibit the IFN-gamma expression and interfere with RIG-1-and STING-mediated signaling through a viral DUB activity. Our study has yielded strong evidence for the TGEV PL1 mechanisms that counteract the host innate immunity.

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