Esterase D enhances type I interferon signal transduction to suppress foot-and-mouth disease virus replication

被引：15

作者：

Li, Weiwei ^{[1
]}

Zhu, Zixiang ^{[1
]}

Cao, Weijun ^{[1
]}

Yang, Fan ^{[1
]}

Zhang, Xiangle ^{[1
]}

Li, Dan ^{[1
]}

Zhang, Keshan ^{[1
]}

Li, Pengfei ^{[1
]}

Mao, Ruoqing ^{[1
]}

Liu, Xiangtao ^{[1
]}

Zheng, Haixue ^{[1
]}

机构：

[1] Chinese Acad Agr Sci, Lanzhou Vet Res Inst, Minist Agr,State Key Lab Vet Etiol Biol, Key Lab Anim Virol,Natl Foot & Mouth Dis Referenc, Lanzhou, Gansu, Peoples R China

来源：

MOLECULAR IMMUNOLOGY | 2016年 / 75卷

关键词：

Foot-and-mouth disease virus; Esterase D; IRF3; Interferon-stimulated genes; Antiviral response; RIG-I; PATHOGEN RECOGNITION; GENE-EXPRESSION; MOLECULAR-BASIS; PROTEIN; SWINE; IDENTIFICATION; INFECTION; CYTOKINE; KINASE;

D O I：

10.1016/j.molimm.2016.05.016

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

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.

引用

页码：112 / 121

页数：10

共 39 条

[1]

Regulation of Signal Transduction by Enzymatically Inactive Antiviral RNA Helicase Proteins MDA5, RIG-I, and LGP2 [J].