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

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

Journal: Journal of virology 2007;81(1):374-83

PMID: 17050612

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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.

Address: Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037, USA.

DOI: 10.1128/JVI.01134-06

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MeSH Terms: Anticholesteremic Agents, Antigens, CD, Cell Line, Cholesterol, Gene Expression Regulation, Hepacivirus, Humans, RNA, Viral, Replicon, Scavenger Receptors, Class B, Tetraspanin 28, beta-Cyclodextrins