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Diverse hepatitis C virus glycoproteins mediate viral infection in a CD81-dependent manner

McKeating, Jane A and Zhang, L Q and Logvinoff, C and Flint, M and Zhang, J and Yu, J and Butera, D and Ho, D D and Dustin, L B and Rice, C M and Balfe, Peter (2004) Diverse hepatitis C virus glycoproteins mediate viral infection in a CD81-dependent manner. Journal of virology, 78 (16). pp. 8496-505. ISSN 0022-538X

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URL of Published Version: http://dx.doi.org/10.1128/JVI.78.16.8496-8505.2004

Identification Number/DOI: 10.1128/JVI.78.16.8496-8505.2004

We recently reported that retroviral pseudotypes bearing the hepatitis C virus (HCV) strain H and Con1 glycoproteins, genotype 1a and 1b, respectively, require CD81 as a coreceptor for virus-cell entry and infection. Soluble truncated E2 cloned from a number of diverse HCV genotypes fail to interact with CD81, suggesting that viruses of diverse origin may utilize different receptors and display altered cell tropism. We have used the pseudotyping system to study the tropism of viruses bearing diverse HCV glycoproteins. Viruses bearing these glycoproteins showed a 150-fold range in infectivity for hepatoma cells and failed to infect lymphoid cells. The level of glycoprotein incorporation into particles varied considerably between strains, generally reflecting the E2 expression level within transfected cells. However, differences in glycoprotein incorporation were not associated with virus infectivity, suggesting that infectivity is not limited by the absolute level of glycoprotein. All HCV pseudotypes failed to infect HepG2 cells and yet infected the same cells after transduction to express human CD81, confirming the critical role of CD81 in HCV infection. Interestingly, these HCV pseudotypes differed in their ability to infect HepG2 cells expressing a panel of CD81 variants, suggesting subtle differences in the interaction of CD81 residues with diverse viral glycoproteins. Our current model of HCV infection suggests that CD81, together with additional unknown liver specific receptor(s), mediate the virus-cell entry process.

Type of Work:Article
Date:2004 (Publication)
School/Faculty:Schools (1998 to 2008) > School of Medicine
Department:Immunity and Infection
Subjects:R Medicine (General)
QR355 Virology
QR180 Immunology
QR Microbiology
Institution:University of Birmingham
Copyright Holders:American Society for Microbiology
ID Code:495
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