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JAC Advance Access published online on May 5, 2004
Journal of Antimicrobial Chemotherapy, doi:10.1093/jac/dkh239
© 2004 by The British Society for Antimicrobial Chemotherapy
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Leading article

CC-chemokine receptor 5 (CCR5) in hepatitis C--at the crossroads of the antiviral immune response?

Golo Ahlenstiel 1, Rainer P. Woitas 1, Jürgen Rockstroh 1, Ulrich Spengler 1*

1 Department of Internal Medicine I, Rheinische Friedrich Wilhelms Universität Bonn, Sigmund-Freud-Straße 25, D-53105 Bonn, Germany

* To whom correspondence should be addressed. E-mail: spengler{at}uni-bonn.de.


  Abstract

An effective immune response to hepatitis C virus (HCV) infection requires efficient recruitment and activation of inflammatory cells to the liver, the site of infection. Chemokines are critically involved in this process, since they exert both chemotactic and immunoregulatory actions. In particular, the interaction between chemokines CCL3 (MIP-1{alpha}), CCL4 (MIP-1{beta}) and CCL5 (RANTES) and their receptor, CC-chemokine receptor 5 (CCR5), may be critical in regulating T cell functions by mediating recruitment, polarization, activation and differentiation of antiviral type 1 cytokine secreting T helper and cytotoxic T cells. A 32 bp deletion in the encoding region of CCR5 leads to complete loss of the functional CCR5 receptor in subjects homozygous for this mutation and decreased expression in heterozygous patients. This fact provides the unique opportunity to study the role of the CCR5 receptor in chronic hepatitis C infection by comparing immune responses between HCV infected CCR5-{Delta}32 carriers and CCR5 wild-type patients. This article will summarize and discuss the available data with respect to possibly altered disease susceptibility, clinical course and treatment outcomes associated with the CCR5-{Delta}32 mutation in hepatitis C.

Key Words: Keywords: HCV, T lymphocytes, mutations


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[Abstract] [Full Text] [PDF]


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