644-M. Does CCR2b-V64I Influence HCV and HCV/HIV Co-Infection?

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Session 85 Poster Session
HCV Co-Infection: Diagnosis and Pathogenesis
Session Time: 4:30-6:30 pm
Room 4E-F

644-M.

Does CCR2b-V64I Influence HCV and HCV/HIV Co-Infection?
G. Ahlenstiel*, R. P. Woitas, J. K. Rockstroh, H. H. Brackmann, B. Kupfer, T. Sauerbruch, and U. Spengler
Univ. of Bonn, Germany

Background: Recently, we observed that the D32-mutation of the chemokine receptor 5, which protects against HIV, is apparently associated with a chronic course of hepatitis C. A different polymorphism, a point mutation in the receptor gene (CCR2b-V64I) for monocyte chemoattractant protein-1 (MCP-1), also leads to delayed progression of human immunodeficiency virus (HIV) infection to AIDS. It is currently unclear, whether this mutation also influences hepatitis C (HCV) infection.
Methods: Since HIV/HCV co-infection is a frequent problem, we investigated prospectively the frequency of the CCR2b-V64I mutation with a real-time PCR hybridization method in patients with HIV/HCV co-infection (n=130), HIV infection (n=105), HCV infection (n=154) and 112 healthy blood donors. We stratified each group into CCR2b-V64I homozygotes, CCR2b-V64I/CCR2b heterozygotes, and CCR2b homozygotes, respectively. The resulting subsets were compared with respect to HIV and HCV loads, CD4 and CD8 cell counts.
Results: CCR2b-V64I homozygosity was found in only 2 patients with HIV-infection (1.9%) and was completely absent in the other groups. Similar frequencies of the mutant allele were found in all groups (HIV/HCV: 25/130=19.2%, HIV: 19/105=18.1%, HCV: 25/154=16.2%, controls: 25/112=22.3%). In neither group CD4 and CD8 counts were affected significantly by the mutation. On average, HIV-infected and HIV/HCV-co-infected patients bearing the mutant allele showed more than 3-fold lower HIV loads (22.9 x 103 vs 6.4 x 103 copies/mL) than CCR2b wildtype patients (ns). Compared to wildtype patients CCR2b-V64I heterozygotes with HCV infection or HIV/HCV coinfection exhibited reduced HCV loads (HCV: CCR2b/CCR2b-V64I vs CCR2b/CCR2b (mean + range): 8.9x106 (100-31.8x106) vs 13.6x106 (100-126.5x106) copies/mL, ns; HIV/HCV: 22.4x106 (100-94.4x106) vs 27.9x106 (100-178.9x106) copies/mL, ns).
Conclusion: Although the CCR2b-V64I mutation may affect HIV- and HCV-loads differentially, our study does not support a close association between hepatitis C and the presence of this polymorphism.

Š2002 9^th Conference on Retroviruses and Opportunistic Infections