Tight junction proteins claudin-1 and occludin control hepatitis C virus entry and are downregulated during infection to prevent superinfection.

Journal Article (Journal Article)

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.

Full Text

Duke Authors

Cited Authors

  • Liu, S; Yang, W; Shen, L; Turner, JR; Coyne, CB; Wang, T

Published Date

  • February 2009

Published In

Volume / Issue

  • 83 / 4

Start / End Page

  • 2011 - 2014

PubMed ID

  • 19052094

Pubmed Central ID

  • PMC2643775

Electronic International Standard Serial Number (EISSN)

  • 1098-5514

Digital Object Identifier (DOI)

  • 10.1128/JVI.01888-08

Language

  • eng

Conference Location

  • United States