Hepatitis C virus (HCV) proliferates by hijacking the host lipid machinery. In vitro replication systems revealed many aspects of the virus life cycle; in particular, viral utilization of host lipid metabolism during HCV proliferation. HCV interacts with lipid droplets (LDs) before starting the process of virus capsid formation at the lipid-rich endoplasmic reticulum (ER) membrane compartment. HCV buds into the ER via lipoprotein assembly and secretion. Exchangeable apolipoproteins, represented by apolipoprotein E (apoE), play pivotal roles in enhancing HCV-specific infectivity. HCV virions are likely to interact with other lipoproteins circulating in blood vessels and incorporate apolipoproteins as well as lipids. This review focuses on virus assembly and egress by briefly describing the recent advances in this area.

中文翻译：

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通过修饰宿主脂质代谢系统进行的HCV组装和出口

丙型肝炎病毒（HCV）通过劫持宿主脂质机制而增殖。体外复制系统揭示了病毒生命周期的许多方面。特别是在HCV增殖过程中宿主脂质代谢的病毒利用。HCV与脂质小滴（LDs）相互作用，然后开始在富含脂质的内质网（ER）膜室中形成病毒衣壳。HCV通过脂蛋白组装和分泌进入ER。以载脂蛋白E（apoE）为代表的可交换载脂蛋白在增强HCV特异性感染力中起关键作用。HCV病毒粒子可能与血管中循环的其他脂蛋白相互作用，并结合载脂蛋白和脂质。本文通过简要介绍该领域的最新进展，重点介绍病毒的组装和出口。