Initiation of hepatitis C virus infection is dependent on cholesterol and cooperativity between CD81 and scavenger receptor B type I
Initiation of hepatitis C virus infection is dependent on cholesterol and cooperativity between CD81 and scavenger receptor B type I
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DOI：
10.1128/jvi.01134-06
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发表时间：
2007-01-01
影响因子：
5.4
通讯作者：
Chisari, Francis V.
中科院分区：
文献类型：
--
作者：
Kapadia, Sharookh B.;Barth, Heidi;Chisari, Francis V.
在过去的几年中，许多细胞蛋白已被确定为候选进入受体的丙型肝炎病毒（HCV）通过使用替代模型的HCV感染。其中，四跨膜蛋白CD 81和清道夫受体B I型（SR-BI），这两个定位于专门的质膜结构域富含胆固醇，已被认为是HCV进入的关键球员。在目前的研究中，我们使用了一个最近开发的体外HCV感染系统，以证明这两个CD 81和SR-BI是需要真实的HCV体外感染，它们的功能合作启动HCV感染，和CD 81介导的HCV进入，在一定程度上，依赖于膜胆固醇。
In the past several years, a number of cellular proteins have been identified as candidate entry receptors for hepatitis C virus (HCV) by using surrogate models of HCV infection. Among these, the tetraspanin CD81 and scavenger receptor B type I (SR-BI), both of which localize to specialized plasma membrane domains enriched in cholesterol, have been suggested to be key players in HCV entry. In the current study, we used a recently developed in vitro HCV infection system to demonstrate that both CD81 and SR-BI are required for authentic HCV infection in vitro, that they function cooperatively to initiate HCV infection, and that CD81-mediated HCV entry is, in part, dependent on membrane cholesterol.