MAVS-mediated host cell defense is inhibited by Borna disease virus
MAVS-mediated host cell defense is inhibited by Borna disease virus
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MAVS 介导的宿主细胞防御被博尔纳病病毒抑制
DOI：
10.1016/j.biocel.2013.05.012
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发表时间：
2013-08-01
影响因子：
4
通讯作者：
Xu, Dakang
中科院分区：
文献类型：
--
作者：
Li, Yujun;Song, Wuqi;Xu, Dakang
病毒通常具有防止宿主细胞凋亡的策略，其拮抗病毒复制。博尔纳病病毒（Borna disease virus，BDV）是一种嗜神经性RNA病毒，可引起非细胞溶解性持续感染。尽管BDV通过（TANK）结合激酶1（TBK-1）相关的BDV P蛋白抑制I型干扰素（IFN），但仍不清楚BDV如何在宿主细胞中存活并建立持续感染。最近，人们已经认识到，通过线粒体抗病毒信号蛋白（MAVS）和RIG-I样受体（RLR）信号通路介导的细胞凋亡是先天免疫反应的重要组成部分。在这项工作中，我们表明，BDV X蛋白与线粒体中的MAVS共定位和相互作用，以阻止程序性细胞死亡。BDV X蛋白介导的细胞凋亡抑制不依赖于I型IFN的产生和NF-κ B活性。用RNA干扰（RNAi）降低BDV X的表达或BDV X的突变增强MAVS诱导的细胞死亡。总的来说，我们的数据提供了新的见解BDV X蛋白如何抑制抗病毒相关的程序性细胞死亡，通过其行动的MAVS功能。皇冠版权所有（c）2013由爱思唯尔有限公司出版。保留所有权利。
Viruses often have strategies for preventing host cell apoptosis, which antagonizes viral replication. Borna disease virus (BDV) is a neurotropic RNA virus that establishes a non-cytolytic persistent infection. Although BDV suppresses type I Interferon (IFN) through (TANK)-binding kinase 1 (TBK-1) associated BDV P protein, it is still unclear how BDV can survive in the host cell and establish a persistent infection. Recently, it has been recognized that mitochondria-mediated apoptosis through the mitochondrial antiviral signaling protein (MAVS) and the RIG-I-like receptor (RLR) signaling pathway is a crucial component of the innate immune response. In this work we show that BDV X protein colocalizes and interacts with MAVS in the mitochondria to block programmed cell death. BDV X protein-mediated inhibition of apoptosis was independent of type I IFN production and NF-kappa B activity. The reduction of BDV X expression with RNA interference (RNAi) or the mutation of BDV X enhanced MAVS-induced cell death. Collectively, our data provide novel insights into how BDV X protein inhibits antiviral-associated programmed cell death, through its action of MAVS function. Crown Copyright (c) 2013 Published by Elsevier Ltd. All rights reserved.