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整合应激反应信号通路对病毒感染及病毒拮抗作用的调控

The Regulation of Integrated Stress Response Signaling Pathway on Viral Infection and Viral Antagonism.

作者信息

Wu Yongshu, Zhang Zhidong, Li Yanmin, Li Yijing

机构信息

State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, China.

College of Veterinary Medicine, Northeast Agricultural University, Harbin, China.

出版信息

Front Microbiol. 2022 Feb 11;12:814635. doi: 10.3389/fmicb.2021.814635. eCollection 2021.

DOI:10.3389/fmicb.2021.814635
PMID:35222313
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8874136/
Abstract

The integrated stress response (ISR) is an adaptational signaling pathway induced in response to different stimuli, such as accumulation of unfolded and misfolded proteins, hypoxia, amino acid deprivation, viral infection, and ultraviolet light. It has been known that viral infection can activate the ISR, but the role of the ISR during viral infection is still unclear. In some cases, the ISR is a protective mechanism of host cells against viral infection, while viruses may hijack the ISR for facilitating their replication. This review highlighted recent advances on the induction of the ISR upon viral infection and the downstream responses, such as autophagy, apoptosis, formation of stress granules, and innate immunity response. We then discussed the molecular mechanism of the ISR regulating viral replication and how viruses antagonize this cellular stress response resulting from the ISR.

摘要

整合应激反应(ISR)是一种适应性信号通路,可响应不同刺激而被诱导,如未折叠和错误折叠蛋白的积累、缺氧、氨基酸剥夺、病毒感染及紫外线照射。已知病毒感染可激活ISR,但ISR在病毒感染过程中的作用仍不清楚。在某些情况下,ISR是宿主细胞抵御病毒感染的一种保护机制,而病毒可能会劫持ISR以促进自身复制。本综述重点介绍了病毒感染后ISR诱导及下游反应(如自噬、凋亡、应激颗粒形成和先天免疫反应)的最新进展。然后我们讨论了ISR调节病毒复制的分子机制以及病毒如何拮抗由ISR引起的这种细胞应激反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f4/8874136/660fa9962f60/fmicb-12-814635-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f4/8874136/19963d2a3a4a/fmicb-12-814635-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f4/8874136/ef43f6b3fd82/fmicb-12-814635-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f4/8874136/7f838e5231ba/fmicb-12-814635-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f4/8874136/660fa9962f60/fmicb-12-814635-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f4/8874136/19963d2a3a4a/fmicb-12-814635-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f4/8874136/ef43f6b3fd82/fmicb-12-814635-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f4/8874136/7f838e5231ba/fmicb-12-814635-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/35f4/8874136/660fa9962f60/fmicb-12-814635-g004.jpg

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