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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Hepatitis C virus production by human hepatocytes dependent on assembly and secretion of very low-density lipoproteins
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Hepatitis C virus production by human hepatocytes dependent on assembly and secretion of very low-density lipoproteins

机译：人肝细胞产生的丙型肝炎病毒取决于极低密度脂蛋白的组装和分泌

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摘要

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.
机译：丙型肝炎病毒（HCV）和富含甘油三酸酯的极低密度脂蛋白（VLDLs）均由肝细胞唯一分泌，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了HCV在其中复制的膜囊泡。这些包含HCV复制复合物的囊泡富含VLDL组装所需的蛋白质，包括载脂蛋白B（apoB），apoE和微粒体甘油三酸酯转移蛋白。在组成性产生感染性HCV的肝癌细胞中，HCV的产生被两种阻止VLDL组装的药物减少：微粒体甘油三酸酯转移蛋白的抑制剂和针对apoB的siRNA。这些结果为限制HCV产生向肝脏提供了可能的解释，并提出了治疗HCV感染的新细胞靶标。

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