André Patrice, Perlemuter Gabriel, Budkowska Agata, Bréchot Christian, Lotteau Vincent
INSERM U503, IFR 128 Biosciences Lyon Gerland, 21 avenue Tony Garnier, 69365 Lyon cedex 07, France.
Semin Liver Dis. 2005 Feb;25(1):93-104. doi: 10.1055/s-2005-864785.
The majority of infectious hepatitis C particles are present in the low-density fractions from plasma of infected patients, suggesting an association of the virus with lipoproteins and the use of lipoprotein receptors for cell entry. Although classical hepatitis C virus (HCV) virions have been reported by some investigators, their role in the HCV life cycle has not been clearly identified. Moreover, two other forms of particles have been characterized: low-density lipo-viro-particles (LVPs) and high-density particles. The latter are nonenveloped nucleocapsids that have immunoglobulin G Fcgamma binding capacity. LVPs are spherical particles enriched in triglycerides. At a minimum, they contain apolipoprotein B, HCV RNA, and core protein. The main source of LVPs is likely to be the enterocytes rather than the hepatocytes, suggesting an interaction between chylomicron and LVP assembly. In experimental systems, HCV core protein inhibits the microsomal triglyceride transfer protein, binds to apolipoprotein AII, and induces accumulation of cytoplasmic lipid droplets. A model of LVP and HCV core-lipid droplet generation is proposed.
大多数丙型肝炎感染性颗粒存在于受感染患者血浆的低密度组分中，这表明该病毒与脂蛋白有关联，且利用脂蛋白受体进入细胞。尽管一些研究人员报告了经典的丙型肝炎病毒（HCV）病毒体，但其在HCV生命周期中的作用尚未明确。此外，还鉴定出了另外两种颗粒形式：低密度脂质病毒颗粒（LVP）和高密度颗粒。后者是具有免疫球蛋白G Fcγ结合能力的无包膜核衣壳。LVP是富含甘油三酯的球形颗粒。它们至少含有载脂蛋白B、HCV RNA和核心蛋白。LVP的主要来源可能是肠上皮细胞而非肝细胞，这表明乳糜微粒与LVP组装之间存在相互作用。在实验系统中，HCV核心蛋白抑制微粒体甘油三酯转移蛋白，与载脂蛋白AII结合，并诱导细胞质脂滴积累。本文提出了LVP和HCV核心 - 脂滴生成的模型。
