Tight Junction Proteins Claudin-1 and Occludin Control Hepatitis C Virus Entry and Are Downregulated during Infection To Prevent Superinfection

被引：267

作者：

Liu, Shufeng

Yang, Wei

Shen, Le ^{[2
]}

Turner, Jerrold R. ^{[2
]}

Coyne, Carolyn B. ^{[3
]}

Wang, Tianyi ^{[1
]}

机构：

[1] Univ Pittsburgh, Grad Sch Publ Hlth, Dept Infect Dis & Microbiol, Pittsburgh, PA 15261 USA

[2] Univ Chicago, Dept Pathol, Chicago, IL 60637 USA

[3] Univ Pittsburgh, Pittsburgh, PA 15261 USA

来源：

JOURNAL OF VIROLOGY | 2009年 / 83卷 / 04期

关键词：

ENDOCYTOSIS; EXPRESSION; MUTATIONS; DISEASE;

D O I：

10.1128/JVI.01888-08

中图分类号：

Q93 [微生物学];

学科分类号：

071005 ; 100705 ;

摘要：

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.

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页码：2011 / 2014

页数：4

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