The Coronavirus PEDV Evades Type III Interferon Response Through the miR-30c-5p/SOCS1 Axis

文献类型： 外文期刊

第一作者： Wang, Changlin

作者： Wang, Changlin;Qu, Shuxin;Wang, Keliang;Wang, Lu;Wang, Ziqi;Xu, Wanhai;Shan, Lingling;Xue, Mei;Fu, Fang;Feng, Li;Liu, Pinghuang

作者机构：

关键词： coronavirus; PEDV; IFN-lambda; SOCS1; microRNA; miR-30c-5p

期刊名称：FRONTIERS IN MICROBIOLOGY （ 影响因子：5.64； 五年影响因子：6.32 ）

ISSN： 1664-302X

年卷期： 2020 年 11 卷

页码：

收录情况： SCI

摘要： Porcine epidemic diarrhea virus (PEDV) is an economically important pathogen that has evolved several mechanisms to evade type I IFN responses. Type III interferon (IFN-lambda), an innate cytokine that primarily targets the mucosal epithelia, is critical in fighting mucosal infection in the host and has been reported to potently inhibit PEDV infection in vitro. However, how PEDV escapes IFN-lambda antiviral response remains unclear. In this study, we found that PEDV infection induced significant IFN-lambda expression in type I IFN-defective Vero E6 cells, but virus-induced endogenous IFN-lambda did not reduce PEDV titers. Moreover, we demonstrated that PEDV escaped IFN-lambda responses by substantially upregulating the suppressor of cytokine signaling protein 1 (SOCS1) expression, which impaired the induction of IFN-stimulated genes (ISGs) and dampened the IFN-lambda antiviral response and facilitated PEDV replication in Vero E6 cells. We further showed that PEDV infection increased SOCS1 expression by decreasing host miR-30c-5p expression. MiR-30c-5p suppressed SOCS1 expression through targeting the 3 ' untranslated region (UTR) of SOCS1. The inhibition of IFN-lambda elicited ISGs expression by SOCS1 was specifically rescued by overexpression of miR-30c-5p. Collectively, our findings identify a new strategy by PEDV to escape IFN-lambda-mediated antiviral immune responses by engaging the SOCS1/miR-30c axis, thus improving our understanding of its pathogenesis.

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