Hepatitis C virus production by human hepatocytes dependent on assembly and secretion of very low-density lipoproteins
Hepatitis C virus production by human hepatocytes dependent on assembly and secretion of very low-density lipoproteins
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DOI：
10.1073/pnas.0700760104
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发表时间：
2007-04-03
影响因子：
11.1
通讯作者：
Ye, Jin
中科院分区：
文献类型：
--
作者：
Huang, Hua;Sun, Fang;Ye, Jin
丙型肝炎病毒（HCV）和富含谷胱甘肽的极低密度脂蛋白（VLDL）都是由肝细胞分泌的，并以复合物的形式在血液中循环。在这里，我们从人肝癌细胞中分离出HCV复制的膜囊泡。这些含有HCV复制复合物的囊泡高度富集VLDL装配所需的蛋白质，包括载脂蛋白B（apoB）、apoE和微粒体甘油三酯转移蛋白。在组成性产生感染性HCV的肝癌细胞中，HCV的产生被两种阻断VLDL组装的试剂减少：微粒体甘油三酯转移蛋白的抑制剂和针对apoB的siRNA。这些结果提供了一个可能的解释限制HCV生产的肝脏，并提出了新的细胞治疗HCV感染的目标。
Hepatitis C virus (HCV) and triglyceride-rich very low-density lipoproteins (VLDLs) both are secreted uniquely by hepatocytes and circulate in blood in a complex. Here, we isolated from human hepatoma cells the membrane vesicles in which HCV replicates. These vesicles, which contain the HCV replication complex, are highly enriched in proteins required for VLDL assembly, including apolipoprotein B (apoB), apoE, and microsomal triglyceride transfer protein. in hepatoma cells that constitutively produce infectious HCV, HCV production is reduced by two agents that block VLDL assembly: an inhibitor of microsomal triglyceride transfer protein and siRNA directed against apoB. These results provide a possible explanation for the restriction of HCV production to the liver and suggest new cellular targets for treatment of HCV infection.