Location of Repository

Initiation of hepatitis C virus infection is dependent on cholesterol and cooperativity between CD81 and scavenger receptor B type I.

By Sharookh B Kapadia, Heidi Barth, Thomas Baumert, Jane A McKeating and Francis V Chisari

Abstract

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

Topics: R Medicine (General), QR355 Virology, QR180 Immunology, QR Microbiology
Year: 2007
OAI identifier: oai:eprints.bham.ac.uk:487

Suggested articles

Preview


To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.