Endoplasmic reticulum stress-mediated autophagy contributes to bluetongue virus infection via the PERK-eIF2 alpha pathway

文献类型： 外文期刊

第一作者： Lv, Shuang

作者： Lv, Shuang;Sun, En-Cheng;Xu, Qing-Yuan;Zhang, Ji-Kai;Wu, Dong-Lai

作者机构：

关键词： Bluetongue virus (BTV);Autophagy;Endoplasmic reticulum (ER) stress;PERK-eIF2 alpha pathway;Replication

期刊名称：BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS （ 影响因子：3.575； 五年影响因子：3.381 ）

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收录情况： SCI

摘要： Bluetongue virus (BTV) is an important pathogen of wild and domestic ruminants. We have previously reported that BTV1 infection induced autophagy for its own benefit, but how this occurs remains unclear. Here, the classical autophagy features including autophagsomes formation, GFP-LC3 dots and LC3-II conversation were shown in BTV1-infected cells, we also found the endoplasmic reticulum (ER) stress was triggered by BTV1 infection, which was demonstrated by the increased transcription level of the ER stress marker GRP78 and the expanded morphology of ER. During ER stress, PERK and eIF2 alpha phosphorylation increased along with BTV1 infection, consistent with the elevated LC3 level, indicating that the PERK pathway of the unfolded protein response (UPR) was activated. In addition, both the blockage of PERK by GSK2656157 or knockdown of eIF2 alpha by siRNA reduced the level of LC3, which suggested that the PERK-eIF2 alpha pathway contributed to autophagy induced by BTV1. Furthermore, inactivation of PERK or silencing of eIF2 alpha both significantly reduced the expression of VP2 protein and the viral yields in the supernatants. In sum, these data suggest that ER stress mediates autophagy via the PERK-eIF2 alpha pathway and contributes to BTV1 replication, thus offering new insight into the molecular mechanisms of the BTV-host interaction. (C) 2015 Elsevier Inc. All rights reserved.

分类号： Q5

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