CHEMOKINE RECEPTOR CCR2B 64I POLYMORPHISM AND ITS RELATION TO CD4 T-CELL COUNTS AND DISEASE PROGRESSION IN A DANISH COHORT OF HIV-INFECTED INDIVIDUALS

Citation
J. Eugenolsen et al., CHEMOKINE RECEPTOR CCR2B 64I POLYMORPHISM AND ITS RELATION TO CD4 T-CELL COUNTS AND DISEASE PROGRESSION IN A DANISH COHORT OF HIV-INFECTED INDIVIDUALS, Journal of acquired immune deficiency syndromes and human retrovirology, 18(2), 1998, pp. 110-116
Citations number
19
Categorie Soggetti
Immunology,"Infectious Diseases
ISSN journal
10779450
Volume
18
Issue
2
Year of publication
1998
Pages
110 - 116
Database
ISI
SICI code
1077-9450(1998)18:2<110:CRC6PA>2.0.ZU;2-U
Abstract
We have investigated the role of the recently described mutation in CC R2b named 64I in relation to HIV resistance, CD4 T-cell counts, and di sease progression in Danish individuals by polymerase chain reaction ( PCR)-based methods as well as sequenced full-length CXCR4 and CCR5 gen es from HIV-infected long-term nonprogressors for possible mutations. In total, 215 Danish individuals were analyzed for 64I allele frequenc y; disease progression was followed in 105 HIV-l-positive homosexual D anish 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 closel y. We found no significant difference in 64I allele frequency between HN-l-seropositive persons (0.08), highrisk HIV-l-seronegative persons (O.11), and blood donors (0.06). No significant difference was observe d 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 alle le carriers and wild-type individuals. Among 9 long-term nonprogressor s, 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 polymorphi sm or other polymorphisms in the CCR5 gene than the CCR5 Delta 32 alle le. Furthermore, we were not able to detect any significant independen t effect of the 64I allele on development to AIDS, overall survival, a nd annual CD4 T-cell decline in this cohort.