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Journal of Virology, April 2007, p. 3693-3703, Vol. 81, No. 8
0022-538X/07/$08.00+0     doi:10.1128/JVI.01748-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Superinfection Exclusion in Cells Infected with Hepatitis C Virus{triangledown}

Donna M. Tscherne,1 Matthew J. Evans,1 Thomas von Hahn,1 Christopher T. Jones,1 Zania Stamataki,2 Jane A. McKeating,2 Brett D. Lindenbach,1 and Charles M. Rice1*

Laboratory of Virology and Infectious Disease, Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, New York 10021,1 Division of Immunity and Infection, Institute of Biomedical Research, University of Birmingham Medical School, Birmingham B15 2TT, United Kingdom2

Received 11 August 2006/ Accepted 29 January 2007

Superinfection exclusion is the ability of an established virus infection to interfere with infection by a second virus. In this study, we found that Huh-7.5 cells acutely infected with hepatitis C virus (HCV) genotype 2a (chimeric strain J6/JFH) and cells harboring HCV genotype 1a, 1b, or 2a full-length or subgenomic replicons were resistant to infection with cell culture-produced HCV (HCVcc). Replicon-containing cells became permissive for HCVcc infection after treatment with an HCV-specific protease inhibitor. With the exception of cells harboring a J6/JFH-FLneo replicon, infected or replicon-containing cells were permissive for HCV pseudoparticle (HCVpp) entry, demonstrating a postentry superinfection block downstream of primary translation. The surprising resistance of J6/JFH-FLneo replicon-containing cells to HCVpp infection suggested a defect in virus entry. This block was due to reduced expression of the HCV coreceptor CD81. Further analyses indicated that J6/JFH may be toxic for cells expressing high levels of CD81, thus selecting for a CD81low population. CD81 down regulation was not observed in acutely infected cells, suggesting that this may not be a general mechanism of HCV superinfection exclusion. Thus, HCV establishes superinfection exclusion at a postentry step, and this effect is reversible by treatment of infected cells with antiviral compounds.

* Corresponding author. Mailing address: Laboratory of Virology and Infectious Diseases, Center for the Study of Hepatitis C, The Rockefeller University, 1230 York Avenue, New York, NY 10021. Phone: (212) 327-7046. Fax: (212) 327-7048. E-mail: ricec{at}mail.rockefeller.edu

{triangledown} Published ahead of print on 7 February 2007.

Journal of Virology, April 2007, p. 3693-3703, Vol. 81, No. 8
0022-538X/07/$08.00+0     doi:10.1128/JVI.01748-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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