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Seneca valley virus activates autophagy through the PERK and ATF6 UPR pathways

文献类型： 外文期刊

作者： Hou, Lei 1 ; Dong, Jianguo 2 ; Zhu, Shanshan 1 ; Yuan, Feng 1 ; Wei, Li 1 ; Wang, Jing 1 ; Quan, Rong 1 ; Chu, Jun 1 ; Wang, 1 ;

作者机构： 1.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing Key Lab Prevent & Control Infect Dis Live, Beijing 100097, Peoples R China

2.Xinyang Agr & Forestry Univ, Coll Anim Husb & Vet Med, Xinyang 464000, Peoples R China

关键词： Seneca valley virus; Autophagy; PERK; ATF6; Viral replication

期刊名称：VIROLOGY （ 影响因子：3.616； 五年影响因子：3.967 ）

ISSN： 0042-6822

年卷期： 2019 年 537 卷

页码：

收录情况： SCI

摘要： Diverse effects on autophagy, a cell degradation pathway, have been associated with the infectious mechanisms of different pathogens. Here, we demonstrated that Seneca valley virus (SVV), an important emerging porcine virus characterized by vesicular lesions and neonatal mortality, can induce autophagy in cultured PK-15 and BHK-21 cells by detecting autophagosome formation, GFP-LC3 puncta and accumulation of LC3-II proteins. Treatment with pharmacological inducers/inhibitors and small interfering RNA sequences targeting genes critical for autophagosome formation affected autophagy induction and viral yields. SVV induced a complete autophagic process to enhance its replication. The PERK and ATF6 pathways, two components of the endoplasmic reticulum (ER)-related unfolded protein response (UPR), were also activated in SVV-infected cells and down-regulation of their expression suppressed SVV-induced autophagy and viral yields. Overall, these results reveal that SVV induces autophagy in cultured cells through the PERK and ATF6 pathways, thereby contributing to understanding of the molecular mechanisms underlying SVV pathogenesis.

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