丙型肝炎病毒 NS5A 在自噬调控中的功能作用

IF 3.3 3区 医学 Q2 MICROBIOLOGY Pathogens Pub Date : 2024-11-08 DOI:10.3390/pathogens13110980
Po-Yuan Ke, Chau-Ting Yeh
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引用次数: 0

摘要

包括丙型肝炎病毒(HCV)在内的许多类型的 RNA 病毒都会激活受感染细胞的自噬作用,以促进病毒生长并对抗宿主的防御反应。自噬是一种分解代谢途径,通过溶酶体清除不必要的物质,从而维持细胞的平衡。HCV 非结构 5A(NS5A)蛋白是一种磷蛋白,病毒 RNA 复制、病毒组装和干扰素(IFN)敏感性的决定都需要它。最近,越来越多的证据表明,HCV NS5A 可诱导自噬,促进线粒体的转换以及肝细胞核因子 1 alpha(HNF-1α)和二酰甘油酰基转移酶 1(DGAT1)的降解。在这篇综述中,我们总结了最近在了解 HCV NS5A 触发自噬的详细机制方面取得的进展,并概述了宿主与病毒之间相互作用平衡的生理意义。
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Functional Role of Hepatitis C Virus NS5A in the Regulation of Autophagy.

Many types of RNA viruses, including the hepatitis C virus (HCV), activate autophagy in infected cells to promote viral growth and counteract the host defense response. Autophagy acts as a catabolic pathway in which unnecessary materials are removed via the lysosome, thus maintaining cellular homeostasis. The HCV non-structural 5A (NS5A) protein is a phosphoprotein required for viral RNA replication, virion assembly, and the determination of interferon (IFN) sensitivity. Recently, increasing evidence has shown that HCV NS5A can induce autophagy to promote mitochondrial turnover and the degradation of hepatocyte nuclear factor 1 alpha (HNF-1α) and diacylglycerol acyltransferase 1 (DGAT1). In this review, we summarize recent progress in understanding the detailed mechanism by which HCV NS5A triggers autophagy, and outline the physiological significance of the balance between host-virus interactions.

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来源期刊
Pathogens
Pathogens Medicine-Immunology and Allergy
CiteScore
6.40
自引率
8.10%
发文量
1285
审稿时长
17.75 days
期刊介绍: Pathogens (ISSN 2076-0817) publishes reviews, regular research papers and short notes on all aspects of pathogens and pathogen-host interactions. There is no restriction on the length of the papers. Our aim is to encourage scientists to publish their experimental and theoretical research in as much detail as possible. Full experimental and/or methodical details must be provided for research articles.
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