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冠状病毒与自噬反应之间的相互作用。

Interaction between coronaviruses and the autophagic response.

作者信息

Yu Jiarong, Ge Shengqiang, Li Jinming, Zhang Yongqiang, Xu Jiao, Wang Yingli, Liu Shan, Yu Xiaojing, Wang Zhiliang

机构信息

China Animal Health and Epidemiology Center, Qingdao, China.

College of Veterinary Medicine, Qingdao Agricultural University, Qingdao, China.

出版信息

Front Cell Infect Microbiol. 2024 Nov 22;14:1457617. doi: 10.3389/fcimb.2024.1457617. eCollection 2024.

DOI:10.3389/fcimb.2024.1457617
PMID:39650836
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11621220/
Abstract

In recent years, the emergence and widespread dissemination of the coronavirus SARS-CoV-2 has posed a significant threat to global public health and social development. In order to safely and effectively prevent and control the spread of coronavirus diseases, a profound understanding of virus-host interactions is paramount. Cellular autophagy, a process that safeguards cells by maintaining cellular homeostasis under diverse stress conditions. Xenophagy, specifically, can selectively degrade intracellular pathogens, such as bacteria, fungi, viruses, and parasites, thus establishing a robust defense mechanism against such intruders. Coronaviruses have the ability to induce autophagy, and they manipulate this pathway to ensure their efficient replication. While progress has been made in elucidating the intricate relationship between coronaviruses and autophagy, a comprehensive summary of how autophagy either benefits or hinders viral replication remains elusive. In this review, we delve into the mechanisms that govern how different coronaviruses regulate autophagy. We also provide an in-depth analysis of virus-host interactions, particularly focusing on the latest data pertaining to SARS-CoV-2. Our aim is to lay a theoretical foundation for the development of novel coronavirus vaccines and the screening of potential drug targets.

摘要

近年来,新型冠状病毒SARS-CoV-2的出现和广泛传播对全球公共卫生和社会发展构成了重大威胁。为了安全有效地预防和控制冠状病毒疾病的传播,深入了解病毒与宿主的相互作用至关重要。细胞自噬是一种在多种应激条件下通过维持细胞内稳态来保护细胞的过程。具体而言,异噬作用可以选择性地降解细胞内病原体,如细菌、真菌、病毒和寄生虫,从而建立起针对此类入侵者的强大防御机制。冠状病毒具有诱导自噬的能力,并且它们操纵这一途径以确保其高效复制。虽然在阐明冠状病毒与自噬之间的复杂关系方面已经取得了进展,但关于自噬如何促进或阻碍病毒复制的全面总结仍然难以捉摸。在这篇综述中,我们深入探讨了不同冠状病毒调节自噬的机制。我们还对病毒与宿主的相互作用进行了深入分析,特别关注与SARS-CoV-2相关的最新数据。我们的目的是为新型冠状病毒疫苗的开发和潜在药物靶点的筛选奠定理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b410/11621220/882f68e062e6/fcimb-14-1457617-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b410/11621220/24bd3613bf50/fcimb-14-1457617-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b410/11621220/30c19a098bfc/fcimb-14-1457617-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b410/11621220/882f68e062e6/fcimb-14-1457617-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b410/11621220/24bd3613bf50/fcimb-14-1457617-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b410/11621220/30c19a098bfc/fcimb-14-1457617-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b410/11621220/882f68e062e6/fcimb-14-1457617-g003.jpg

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本文引用的文献

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Autophagy is induced by swine acute diarrhea syndrome coronavirus through the cellular IRE1-JNK-Beclin 1 signaling pathway after an interaction of viral membrane-associated papain-like protease and GRP78.自噬是由猪急性腹泻综合征冠状病毒通过病毒膜相关的木瓜蛋白酶样蛋白酶与 GRP78 相互作用后,细胞 IRE1-JNK-Beclin 1 信号通路诱导的。
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SARS-CoV-2 Harnesses Host Translational Shutoff and Autophagy To Optimize Virus Yields: the Role of the Envelope (E) Protein.SARS-CoV-2 利用宿主翻译关闭和自噬来优化病毒产量:包膜 (E) 蛋白的作用。
Microbiol Spectr. 2023 Feb 14;11(1):e0370722. doi: 10.1128/spectrum.03707-22. Epub 2023 Jan 9.
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Swine acute diarrhea syndrome coronavirus induces autophagy to promote its replication via the Akt/mTOR pathway.猪急性腹泻综合征冠状病毒通过Akt/mTOR途径诱导自噬以促进其复制。
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MERS-CoV nsp1 regulates autophagic flux via mTOR signalling and dysfunctional lysosomes.中东呼吸综合征冠状病毒 nsp1 通过 mTOR 信号通路和功能失调的溶酶体来调节自噬流。
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Subversion of autophagy machinery and organelle-specific autophagy by SARS-CoV-2 and coronaviruses.SARS-CoV-2 和冠状病毒对自噬机制和细胞器特异性自噬的颠覆作用。
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Autophagy Hijacking in PBMC From COVID-19 Patients Results in Lymphopenia.COVID-19 患者 PBMC 中的自噬劫持导致淋巴细胞减少症。
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The Interplay Between Coronavirus and Type I IFN Response.冠状病毒与I型干扰素反应之间的相互作用
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SARS-CoV-2 ORF3a induces RETREG1/FAM134B-dependent reticulophagy and triggers sequential ER stress and inflammatory responses during SARS-CoV-2 infection.SARS-CoV-2 的 ORF3a 诱导 RETREG1/FAM134B 依赖性的内质网自噬,并在 SARS-CoV-2 感染过程中引发连续的内质网应激和炎症反应。
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SARS-CoV-2 infection enhances mitochondrial PTP complex activity to perturb cardiac energetics.严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染会增强线粒体通透性转换孔(PTP)复合体的活性,从而扰乱心脏能量代谢。
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SARS-CoV-2 NSP13 Inhibits Type I IFN Production by Degradation of TBK1 via p62-Dependent Selective Autophagy.SARS-CoV-2 NSP13 通过 p62 依赖性选择性自噬降解 TBK1 抑制 I 型 IFN 产生。
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