Share this article on:

Chemokine Receptor CCR2b 64I Polymorphism and Its Relation to CD4 T-Cell Counts and Disease Progression in a Danish Cohort of HIV-Infected Individuals

Eugen-Olsen, Jesper; Iversen, Astrid K. N.; Benfield, Thomas L.; Koppelhus, Uffe; Garred, Peter; for the Copenhagen AIDS Cohort
JAIDS Journal of Acquired Immune Deficiency Syndromes: June 1st, 1998
Articles: PDF Only

Summary:We have investigated the role of the recently described mutation in CCR2b named 64I in relation to HIV resistance, CD4 T-cell counts, and disease progression in Danish individuals by polymerase chain reaction (PCR)-based methods as well as sequenced full-length CXCR4 and CCR5 genes from HIV-infected long-term nonprogressors for possible mutations. In total, 215 Danish individuals were analyzed for 64I allele frequency; disease progression was followed in 105 HIV-1-positive homosexual Danish men from their first known positive HIV-1 test result and up to 11 years. In 87 individuals, the CD4 T-cell count was monitored closely. We found no significant difference in 64I allele frequency between HIV-1-seropositive persons (0.08), highrisk HIV-1-seronegative persons (0.11), and blood donors (0.06). No significant difference was observed in annual CD4 T-cell decline, CD4 T-cell counts at the time of AIDS, in AIDS-free survival as well as survival with AIDS, between 64I allele carriers and wild-type individuals. Among 9 long-term nonprogressors, 2 carried the 64I allele, while none of 9 fast progressors carried the 64I allele. However, this was not significantly different (p = .47). Long-term nonprogression could not be explained by CXCR4 polymorphism or other polymorphisms in the CCR5 gene than the CCR5Δ32 allele. Furthermore, we were not able to detect any significant independent effect of the 64I allele on development to AIDS, overall survival, and annual CD4 T-cell decline in this cohort.

Address correspondence and reprint requests to Jesper Eugen-Olsen, Department of Infectious Diseases 144, Copenhagen University Hospitals, Hvidovre, DK-2650, Denmark; email: jeo@biobase.dk

Manuscript received December 12, 1997; accepted February 18, 1998.

© Lippincott-Raven Publishers.