The Journal of Experimental Medicine
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Published 2 August 2004. doi:10.1084/jem.20040638
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 3, 307-319
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Limited T Cell Receptor Diversity of HCV-specific T Cell Responses Is Associated with CTL Escape

Dirk Meyer-Olson1, Naglaa H. Shoukry2, Kristen W. Brady4, Helen Kim1, Douglas P. Olson1, Kelly Hartman1, Ayumi K. Shintani5, Christopher M. Walker2,3, and Spyros A. Kalams1,4,6

1 Partners AIDS Research Center, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02129
2 The Center for Vaccines and Immunity, Columbus Children's Research Institute and 3 Department of Pediatrics, College of Medicine and Public Health, The Ohio State University, Columbus, OH 43205
4 Infectious Diseases Unit, Department of Internal Medicine, 5 Department of General Internal Medicine, Center for Health Services Research, and 6 Department of Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232

Address correspondence to Spyros A. Kalams, Infectious Diseases Unit, Dept. of Internal Medicine and Dept. of Microbiology and Immunology, Vanderbilt University Medical Center, MCN A4103, Nashville, TN 37232. Phone: (615) 322-2035; Fax: (615) 343-6160; email: spyros.a.kalams{at}vanderbilt.edu

Escape mutations are believed to be important contributors to immune evasion by rapidly evolving viruses such as hepatitis C virus (HCV). We show that the majority of HCV-specific cytotoxic T lymphocyte (CTL) responses directed against viral epitopes that escaped immune recognition in HCV-infected chimpanzees displayed a reduced CDR3 amino acid diversity when compared with responses in which no CTL epitope variation was detected during chronic infection or with those associated with protective immunity. Decreased T cell receptor (TCR) CDR3 amino acid diversity in chronic infection could be detected long before the appearance of viral escape mutations in the plasma. In both chronic and resolved infection, identical T cell receptor clonotypes were present in liver and peripheral blood. These findings provide a deeper understanding of the evolution of CTL epitope variations in chronic viral infections and highlight the importance of the generation and maintenance of a diverse TCR repertoire directed against individual epitopes.

Key Words: CD8+ T lymphocytes • CD4+ T lymphocytes • hepatitis C • antigenic variation • epitopes

Abbreviations used in this paper: HCV, hepatitis C virus; TRBJ, T cell receptor ß joining; TRBV, T cell receptor ß variable.


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