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

Academic Article
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Overview

authors

  • Kapadia, S. B.
  • Barth, H.
  • Baumert, T.
  • McKeating, J. A.
  • Chisari, Francis

publication date

  • January 2007

journal

  • Journal of Virology  Journal

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.

subject areas

  • Anticholesteremic Agents
  • Antigens, CD
  • Antigens, CD81
  • Cell Line
  • Cholesterol
  • Gene Expression Regulation
  • Hepacivirus
  • Humans
  • RNA, Viral
  • Replicon
  • Scavenger Receptors, Class B
  • beta-Cyclodextrins
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Identity

International Standard Serial Number (ISSN)

  • 0022-538X

Digital Object Identifier (DOI)

  • 10.1128/jvi.01134-06

PubMed ID

  • 17050612
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Additional Document Info

start page

  • 374

end page

  • 383

volume

  • 81

issue

  • 1

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