Enterovirus 71 inhibits cellular type I interferon signaling by inhibiting host RIG-I ubiquitination
Enterovirus 71 inhibits cellular type I interferon signaling by inhibiting host RIG-I ubiquitination
复制标题
肠道病毒 71 通过抑制宿主 RIG-I 泛素化来抑制细胞 I 型干扰素信号传导
DOI：
10.1016/j.micpath.2016.09.001
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发表时间：
2016-11-01
影响因子：
3.8
通讯作者：
Zhang, Hua
中科院分区：
文献类型：
--
作者：
Chen, Ning;Li, Xingzhi;Zhang, Hua
肠道病毒71型（EV 71）是一种人类病原体，可引起幼儿和婴儿的手足口病（HFMD）和致命的神经系统疾病。EV 71的致病性可能与其通过抑制细胞I型干扰素信号传导逃避宿主先天免疫的能力有关。然而，这是不太好理解的分子事件，管理这一过程。在本研究中，我们发现EV 71感染通过在病毒感染后期抑制IFN-β和IFN刺激基因（ISG）（如ISG 54和ISG 56）的表达水平来抑制抗病毒免疫的诱导。同时，我们的研究结果表明，EV 71感染显著抑制RIG-I的泛素化。相反，RIG-I泛素化的上调促进IFN-β和ISG的表达，表明细胞I型干扰素信号传导的抑制是由EV 71感染期间RIG-I泛素化的下调引起的。这些结果表明，抑制RIG-I介导的I型IFN反应的EV 71可能有助于病毒感染的发病机制。(C)2016爱思唯尔有限公司版权所有。
Enterovirus 71 (EV71) is a human pathogen that induces hand, foot, and mouth disease (HFMD) and fatal neurological diseases in young children and infants. Pathogenicity of EV71 is likely related to its ability to evade host innate immunity through inhibiting cellular type I interferon signaling. However, it is less well understood the molecular events governing this process. In this study, we found that EV71 infection suppressed the induction of antiviral immunity by inhibiting the expression levels of IFN-beta and IFN-stimulated genes (ISGs), such as ISG54 and ISG56, at the late stage of viral infection. At the same time, our results showed that EV71 infection significantly inhibited ubiquitination of RIG-I. In contrast, up regulation of RIG-I ubiquitination promoted expression of IFN-beta and ISGs, suggesting that inhibition of cellular type I interferon signaling was caused by down-regulation of RIG-I ubiquitination during EV71 infection. These results suggest that inhibition of RIG-I-mediated type I IFN responses by EV71 may contribute to the pathogenesis of viral infection. (C) 2016 Elsevier Ltd. All rights reserved.