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Rotavirus VP3 targets MAVS for degradation to inhibit type III interferon expression in intestinal epithelial cells

文献类型： 外文期刊

作者： Din, Siyuan 1 ; Zhu, Shu 4 ; Ren, Lili 1 ; Feng, Ningguo 1 ; Song, Yanhua 1 ; Ge, Xiaomei 3 ; Li, Bin 6 ; Flavell, Richar 1 ;

作者机构： 1.Stanford Univ, Dept Med, Div Gastroenterol & Hepatol, Stanford, CA 94305 USA

2.Stanford Univ, Dept Microbiol & Immunol, Stanford, CA 94305 USA

3.VA Palo Alto Hlth Care Syst, Palo Alto Vet Inst Res, Palo Alto, CA 94304 USA

4.Univ Sci & Technol China, Sch Life Sci & Med Ctr, Inst Immunol, CAS Key Lab Innate Immun & Chron Dis, Hefei, Anhui, Peoples R China

5.Nanjing Tech Univ, Sch Pharmaceut Sci, Nanjing, Jiangsu, Peoples R China

6.Jiangsu Acad Agr Sci, Inst Vet Med, Nanjing, Jiangsu, Peoples R China

7.Stanford Univ, Dept Med, Div Hematol, Stanford, CA 94305 USA

8.Yale Univ, Dept Immunobiol, New Haven, CT USA

9.Howard Hughes Med Inst, Chevy Chase, MD USA

10.Eureka Therapeut Inc, Emeryville, CA USA

期刊名称：ELIFE （ 影响因子：8.14； 五年影响因子：9.056 ）

ISSN： 2050-084X

年卷期： 2018 年 7 卷

页码：

收录情况： SCI

摘要： Rotaviruses (RVs), a leading cause of severe diarrhea in young children and many mammalian species, have evolved multiple strategies to counteract the host innate immunity, specifically interferon (IFN) signaling through RV non-structural protein 1 (NSP1). However, whether RV structural components also subvert antiviral response remains under-studied. Here, we found that MAVS, critical for the host RNA sensing pathway upstream of IFN induction, is degraded by the RV RNA methyl- and guanylyl-transferase (VP3) in a host-range-restricted manner. Mechanistically, VP3 localizes to the mitochondria and mediates the phosphorylation of a previously unidentified SPLTSS motif within the MAVS proline-rich region, leading to its proteasomal degradation and blockade of IFN-lambda production in RV-infected intestinal epithelial cells. Importantly, VP3 inhibition of MAVS activity contributes to enhanced RV replication and to viral pathogenesis in vivo. Collectively, our findings establish RV VP3 as a viral antagonist of MAVS function in mammals and uncover a novel pathogen-mediated inhibitory mechanism of MAVS signaling.

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