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肠道病毒对细胞凋亡的调控

Regulation of Apoptosis by Enteroviruses.

作者信息

Lai Yalan, Wang Mingshu, Cheng Anchun, Mao Sai, Ou Xumin, Yang Qiao, Wu Ying, Jia Renyong, Liu Mafeng, Zhu Dekang, Chen Shun, Zhang Shaqiu, Zhao Xin-Xin, Huang Juan, Gao Qun, Wang Yin, Xu Zhiwen, Chen Zhengli, Zhu Ling, Luo Qihui, Liu Yunya, Yu Yanling, Zhang Ling, Tian Bin, Pan Leichang, Rehman Mujeeb Ur, Chen Xiaoyue

机构信息

Institute of Preventive Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.

Key Laboratory of Animal Disease and Human Health of Sichuan Province, Sichuan Agricultural University, Chengdu, China.

出版信息

Front Microbiol. 2020 Jun 3;11:1145. doi: 10.3389/fmicb.2020.01145. eCollection 2020.

DOI:10.3389/fmicb.2020.01145
PMID:32582091
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7283464/
Abstract

Enterovirus infection can cause a variety of diseases and severely impair the health of humans, animals, poultry, and other organisms. To resist viral infection, host organisms clear infected cells and viruses via apoptosis. However, throughout their long-term competition with host cells, enteroviruses have evolved a series of mechanisms to regulate the balance of apoptosis in order to replicate and proliferate. In the early stage of infection, enteroviruses mainly inhibit apoptosis by regulating the PI3K/Akt pathway and the autophagy pathway and by impairing cell sensors, thereby delaying viral replication. In the late stage of infection, enteroviruses mainly regulate apoptotic pathways and the host translation process via various viral proteins, ultimately inducing apoptosis. This paper discusses the means by which these two phenomena are balanced in enteroviruses to produce virus-favoring conditions - in a temporal sequence or through competition with each other. This information is important for further elucidation of the relevant mechanisms of acute infection by enteroviruses and other members of the picornavirus family.

摘要

肠道病毒感染可引发多种疾病,并严重损害人类、动物、家禽及其他生物体的健康。为抵御病毒感染,宿主生物体通过细胞凋亡清除受感染的细胞和病毒。然而,在与宿主细胞的长期竞争过程中,肠道病毒已进化出一系列调节细胞凋亡平衡的机制,以便进行复制和增殖。在感染早期,肠道病毒主要通过调节PI3K/Akt通路和自噬通路以及损害细胞传感器来抑制细胞凋亡,从而延迟病毒复制。在感染后期,肠道病毒主要通过各种病毒蛋白调节凋亡通路和宿主翻译过程,最终诱导细胞凋亡。本文讨论了肠道病毒如何平衡这两种现象以产生有利于病毒的条件——按时间顺序或通过相互竞争。这些信息对于进一步阐明肠道病毒及微小核糖核酸病毒科其他成员急性感染的相关机制具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/f4bde0d383f7/fmicb-11-01145-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/287e367b1aee/fmicb-11-01145-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/fa54c6cf9154/fmicb-11-01145-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/fda9c891f2fb/fmicb-11-01145-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/d53de0cbf163/fmicb-11-01145-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/f4bde0d383f7/fmicb-11-01145-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/287e367b1aee/fmicb-11-01145-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/fa54c6cf9154/fmicb-11-01145-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/fda9c891f2fb/fmicb-11-01145-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/d53de0cbf163/fmicb-11-01145-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b720/7283464/f4bde0d383f7/fmicb-11-01145-g005.jpg

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本文引用的文献

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Apoptosis and Autophagy in Picornavirus Infection.微小核糖核酸病毒感染中的细胞凋亡与自噬
Front Microbiol. 2019 Sep 3;10:2032. doi: 10.3389/fmicb.2019.02032. eCollection 2019.
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EV71 3C protease induces apoptosis by cleavage of hnRNP A1 to promote apaf-1 translation.肠道病毒 71 型 3C 蛋白酶通过切割 hnRNP A1 诱导细胞凋亡,从而促进凋亡酶激活因子 1 的翻译。
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Seneca Valley Virus 2C and 3C Induce Apoptosis via Mitochondrion-Mediated Intrinsic Pathway.
全外显子组测序鉴定东亚人群肠道病毒易感性的遗传标志物。
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Viroporins Manipulate Cellular Powerhouses and Modulate Innate Immunity.病毒离子通道蛋白操控细胞的能量工厂并调节先天免疫。
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The role of non-coding RNAs in myocarditis: a narrative review.非编码RNA在心肌炎中的作用:一篇叙述性综述。
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Advances in cell death mechanisms involved in viral myocarditis.病毒性心肌炎中细胞死亡机制的研究进展。
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Dual inhibition of innate immunity and apoptosis by human cytomegalovirus protein UL37x1 enables efficient virus replication.人巨细胞病毒蛋白 UL37x1 对固有免疫和细胞凋亡的双重抑制作用使病毒能够高效复制。
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