Tight Junction Proteins Claudin-1 and Occludin Control Hepatitis C Virus Entry and Are Downregulated during Infection To Prevent Superinfection
Tight Junction Proteins Claudin-1 and Occludin Control Hepatitis C Virus Entry and Are Downregulated during Infection To Prevent Superinfection
复制标题
DOI：
10.1128/jvi.01888-08
复制
发表时间：
2009-02-15
影响因子：
5.4
通讯作者：
Wang, Tianyi
中科院分区：
文献类型：
--
作者：
Liu, Shufeng;Yang, Wei;Wang, Tianyi
紧密连接(TJ)蛋白Claudin-1(CLDN1)最近被确定为丙型肝炎病毒(HCV)进入的关键因素。在这里，我们展示了另一种TJ蛋白，occludin，也是丙型肝炎病毒进入所必需的。CLDN1的突变研究表明，其紧密的连接分布在介导病毒进入中起着重要作用。总之，这些数据支持丙型肝炎病毒从TJ进入肝细胞的模型。有趣的是，丙型肝炎病毒感染Huh-7肝癌细胞，下调了CLDN1和occludin的表达，防止了重叠感染。TJ蛋白表达的改变可能与观察到的丙型肝炎病毒感染肝细胞的形态和功能改变有关。
A tight junction (TJ) protein, claudin-1 (CLDN1), was identified recently as a key factor for hepatitis C virus (HCV) entry. Here, we show that another TJ protein, occludin, is also required for HCV entry. Mutational study of CLDN1 revealed that its tight junctional distribution plays an important role in mediating viral entry. Together, these data support the model in which HCV enters liver cells from the TJ. Interestingly, HCV infection of Huh-7 hepatoma cells downregulated the expression of CLDN1 and occludin, preventing superinfection. The altered TJ protein expression may contribute to the morphological and functional changes observed in HCV-infected hepatocytes.