Pécheur Eve-Isabelle
Department of Mechanisms of Chronic Hepatitis B and C, Centre de Recherche en Cancérologie de Lyon, 69008 Lyon, France ; Inserm U1052/CNRS UMR 5286, CRCL, Université de Lyon, 151 Cours Albert Thomas, 69424 Lyon Cedex 03, France.
Scientifica (Cairo). 2012;2012:709853. doi: 10.6064/2012/709853. Epub 2012 Dec 23.
Viruses are obligate intracellular agents that depend on host cells for successful propagation, hijacking cellular machineries to their own profit. The molecular interplay between host factors and invading viruses is a continuous coevolutionary process that determines viral host range and pathogenesis. The hepatitis C virus (HCV) is a strictly human pathogen, causing chronic liver injuries accompanied by lipid disorders. Upon infection, in addition to protein-protein and protein-RNA interactions usual for such a positive-strand RNA virus, HCV relies on protein-lipid interactions at multiple steps of its life cycle to establish persistent infection, making use of hepatic lipid pathways. This paper focuses on lipoproteins in HCV entry and on receptors and enzymes involved in lipid metabolism that HCV exploits to enter hepatocytes.
病毒是专性细胞内病原体,依靠宿主细胞才能成功繁殖,它们劫持细胞机制为自身谋利。宿主因子与入侵病毒之间的分子相互作用是一个持续的共同进化过程,决定了病毒的宿主范围和发病机制。丙型肝炎病毒(HCV)是一种严格的人类病原体,会导致伴有脂质紊乱的慢性肝损伤。感染后,除了这种正链RNA病毒常见的蛋白质-蛋白质和蛋白质-RNA相互作用外,HCV在其生命周期的多个步骤中依赖蛋白质-脂质相互作用,利用肝脏脂质途径建立持续感染。本文重点关注HCV进入过程中的脂蛋白以及HCV用于进入肝细胞的脂质代谢相关受体和酶。