Journal
JOURNAL OF VIROLOGY
Volume 81, Issue 1, Pages 374-383Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01134-06
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Funding
- NATIONAL CANCER INSTITUTE [R01CA108304] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI050798] Funding Source: NIH RePORTER
- MRC [G0400802] Funding Source: UKRI
- Medical Research Council [G0801976, G0400802] Funding Source: Medline
- NCI NIH HHS [R01 CA108304, CA108304] Funding Source: Medline
- NIAID NIH HHS [R01 AI050798, AI50798] Funding Source: Medline
- Medical Research Council [G9818340B] Funding Source: researchfish
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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.
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