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Journal of Virology, April 2005, p. 4870-4876, Vol. 79, No. 8
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.8.4870-4876.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Escape Mutations Alter Proteasome Processing of Major Histocompatibility Complex Class I-Restricted Epitopes in Persistent Hepatitis C Virus Infection

Yoichi Kimura,1 Toshifumi Gushima,1 Sharad Rawale,2 Pravin Kaumaya,2 and Christopher M. Walker1,3*

Center for Vaccines and Immunity, The Columbus Children's Research Institute,1 Departments of Obstetrics and Gynecology,2 Pediatrics, The Ohio State University, Columbus, Ohio3

Received 11 July 2004/ Accepted 30 November 2004

Mutations in hepatitis C virus (HCV) genomes facilitate escape from virus-specific CD8+ T lymphocytes in persistently infected chimpanzees. Our previous studies demonstrated that many of the amino acid substitutions in HCV epitopes prevented T-cell receptor recognition or binding to class I major histocompatibility complex molecules. Here we report that mutations within HCV epitopes also cause their destruction by changing the pattern of proteasome digestion. This mechanism of immune evasion provides further evidence of the potency of CD8+ T-cell selection pressure against HCV and should be considered when evaluating the significance of mutations in viral genomes from persistently infected chimpanzees and humans.

* Corresponding author. Mailing address: Children's Hospital, WA4011, 700 Children's Dr., Columbus, OH 43205. Phone: (614) 722-2692. Fax: (614) 722-3680. E-mail: WalkerC{at}pediatrics.ohio-state.edu.

Journal of Virology, April 2005, p. 4870-4876, Vol. 79, No. 8
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.8.4870-4876.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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