Hijacking autophagy for infection by flaviviruses

IF 2.5 4区 医学 Q3 VIROLOGY
Ming-Hui Song , Yan Sun , Xiao-Bo Qiu
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引用次数: 0

Abstract

Autophagy is a lysosomal degradative pathway, which regulates the homeostasis of eukaryotic cells. This pathway can degrade misfolded or aggregated proteins, clear damaged organelles, and eliminate intracellular pathogens, including viruses, bacteria, and parasites. But, not all types of viruses are eliminated by autophagy. Flaviviruses (e.g., Yellow fever, Japanese encephalitis, Hepatitis C, Dengue, Zika, and West Nile viruses) are single-stranded and enveloped RNA viruses, and transmitted to humans primarily through the bites of arthropods, leading to severe and widespread illnesses. Like the coronavirus SARS-CoV-II, flaviviruses hijack autophagy for their infection and escape from host immune clearance. Thus, it is possible to control these viral infections by inhibiting autophagy. In this review, we summarize recent research progresses on hijacking of autophagy by flaviviruses and discuss the feasibility of antiviral therapies using autophagy inhibitors.

Abstract Image

劫持自噬以感染黄病毒
自噬是一种溶酶体降解途径,可调节真核细胞的平衡。这种途径可以降解折叠错误或聚集的蛋白质,清除受损细胞器,并消除细胞内的病原体,包括病毒、细菌和寄生虫。但并非所有类型的病毒都能被自噬消除。黄病毒(如黄热病、日本脑炎、丙型肝炎、登革热、寨卡病毒和西尼罗河病毒)是单链和包膜 RNA 病毒,主要通过节肢动物叮咬传播给人类,导致严重和广泛的疾病。与冠状病毒 SARS-CoV-II 一样,黄病毒也会劫持自噬来进行感染,并逃避宿主的免疫清除。因此,有可能通过抑制自噬来控制这些病毒感染。在这篇综述中,我们总结了黄病毒劫持自噬的最新研究进展,并讨论了使用自噬抑制剂进行抗病毒治疗的可行性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Virus research
Virus research 医学-病毒学
CiteScore
9.50
自引率
2.00%
发文量
239
审稿时长
43 days
期刊介绍: Virus Research provides a means of fast publication for original papers on fundamental research in virology. Contributions on new developments concerning virus structure, replication, pathogenesis and evolution are encouraged. These include reports describing virus morphology, the function and antigenic analysis of virus structural components, virus genome structure and expression, analysis on virus replication processes, virus evolution in connection with antiviral interventions, effects of viruses on their host cells, particularly on the immune system, and the pathogenesis of virus infections, including oncogene activation and transduction.
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