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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board Member: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Sies, Helmut / Turk, Boris / Wittinghofer, Alfred

SCImago Journal Rank (SJR) 2015: 1.607
Source Normalized Impact per Paper (SNIP) 2015: 0.751
Impact per Publication (IPP) 2015: 2.609

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Adaptive immune responses to hepatitis C virus: from viral immunobiology to a vaccine

Robert Thimme1 / Christoph Neumann-Haefelin2 / Tobias Boettler3 / Hubert E. Blum4

1Department of Medicine II, University Hospital Freiburg, D-79106 Freiburg, Germany

2Department of Medicine II, University Hospital Freiburg, D-79106 Freiburg, Germany

3Department of Medicine II, University Hospital Freiburg, D-79106 Freiburg, Germany

4Department of Medicine II, University Hospital Freiburg, D-79106 Freiburg, Germany

Corresponding author

Citation Information: Biological Chemistry. Volume 389, Issue 5, Pages 457–467, ISSN (Online) 14374315, ISSN (Print) 1431-6730, DOI: 10.1515/BC.2008.061, March 2008

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Hepatitis C virus (HCV) causes chronic infection in approximately two-thirds of cases, leading to chronic hepatitis, liver cirrhosis, liver disease, liver failure, and hepatocellular carcinoma in a substantial proportion of the 170 million HCV-infected individuals worldwide. It is generally accepted that the cellular immune response plays the most important role in determining the outcome of HCV infection. First, vigorous, multispecific and sustained CD4+ and CD8+ T-cell responses are associated with viral clearance. Second, depletion studies in chimpanzees, the only other host of HCV besides humans, have shown that both CD4+ and CD8+ T-cells are required for virus elimination. Third, the host's human leukocyte antigen alleles, which restrict the repertoire of CD4+ and CD8+ T-cell responses, influence the outcome of infection. Of note, protective immunity has been demonstrated in population-based studies, as well as in experimentally infected chimpanzees. Thus, a detailed understanding of the mechanisms contributing to the failure of the antiviral immune response should allow successful development of prophylactic and therapeutic vaccination strategies.

Keywords: hepatitis; immune response; T-cells; viral escape

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