Ke Po-Yuan
Department of Biochemistry & Molecular Biology and Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan.
Liver Research Center, Chang Gung Memorial Hospital, Taoyuan 33305, Taiwan.
Pathogens. 2024 Mar 20;13(3):266. doi: 10.3390/pathogens13030266.
Autophagy plays a fundamental role in maintaining cellular homeostasis by eliminating intracellular components via lysosomes. Successful degradation through autophagy relies on the fusion of autophagosomes to lysosomes, which leads to the formation of autolysosomes containing acidic proteases that degrade the sequestered materials. Viral infections can exploit autophagy in infected cells to balance virus-host cell interactions by degrading the invading virus or promoting viral growth. In recent years, cumulative studies have indicated that viral infections may interfere with the fusion of autophagosomes and lysosomes, thus benefiting viral replication and associated pathogenesis. In this review, I provide an overview of the current understanding of the molecular mechanism by which human viral infections deregulate autophagosome-lysosome fusion and summarize the physiological significance in the virus life cycle and host cell damage.
自噬通过溶酶体清除细胞内成分，在维持细胞内稳态中发挥着基本作用。自噬的成功降解依赖于自噬体与溶酶体的融合，这导致形成含有酸性蛋白酶的自噬溶酶体，从而降解被隔离的物质。病毒感染可利用受感染细胞中的自噬，通过降解入侵病毒或促进病毒生长来平衡病毒与宿主细胞的相互作用。近年来，越来越多的研究表明，病毒感染可能会干扰自噬体与溶酶体的融合，从而有利于病毒复制和相关发病机制。在这篇综述中，我概述了目前对人类病毒感染失调自噬体 - 溶酶体融合分子机制的理解，并总结了其在病毒生命周期和宿主细胞损伤中的生理意义。
