Esterase D enhances type I interferon signal transduction to suppress foot-and-mouth disease virus replication
文献类型: 外文期刊
第一作者: Li, Weiwei
作者: Li, Weiwei;Zhu, Zixiang;Cao, Weijun;Yang, Fan;Zhang, Xiangle;Li, Dan;Zhang, Keshan;Li, Pengfei;Mao, Ruoqing;Liu, Xiangtao;Zheng, Haixue
作者机构:
关键词: Foot-and-mouth disease virus;Esterase D;IRF3;Interferon-stimulated genes;Antiviral response
期刊名称:MOLECULAR IMMUNOLOGY ( 影响因子:4.407; 五年影响因子:4.227 )
ISSN:
年卷期:
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收录情况: SCI
摘要: The enzymatic activities of esterase D (ESD) are involved in many human diseases. However, no antiviral property of ESD has been described to date. Foot-and-mouth disease virus (FMDV) is the etiological agent of foot-and-mouth disease. In this study, we showed that FMDV infection triggered ESD expression. Over expression of ESD significantly suppressed FMDV replication and knockdown of ESD expression enhanced virus replication, showing an essential antiviral role of ESD. Furthermore, we found that Sendai-virus induced interferon (IFN) signaling was enhanced by upregulation of ESD, and ESD promoted activation of the IFN-beta promoter simulated by IFN regulatory factor (IRF)3 or its upstream molecules (retinoic acid-inducible gene-I, melanoma differentiation-associated protein 5, virus-induced signaling adaptor and TANK binding kinase 1). Detailed analysis revealed that ESD protein enhanced IRF3 phosphorylation during FMDV infection. Overexpression of ESD also promoted the expression of various antiviral interferon-stimulated genes (ISGs) and knockdown of ESD impaired the expression of these antiviral genes during FMDV infection. Our findings demonstrate a new mechanism evolved by ESD to enhance type I IFN signal transduction and suppress viral replication during FMDV infection. (C) 2016 Elsevier Ltd. All rights reserved.
分类号: R392
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