@article{3004674,
    title = "CCR2-64I and CXCL12 3′A alleles confer a favorable prognosis to AIDS patients undergoing HAART therapy",
    author = "Passam, A.M. and Zafiropoulos, A. and Miyakis, S. and Zagoreos, I. and Stavrianeas, N.G. and Krambovitis, E. and Spandidos, D.A.",
    journal = "Journal of Clinical Virology",
    year = "2005",
    volume = "34",
    number = "4",
    pages = "302-309",
    issn = "1386-6532",
    doi = "10.1016/j.jcv.2004.05.021",
    keywords = "antiretrovirus agent;  RNA directed DNA polymerase inhibitor, acquired immune deficiency syndrome;  adult;  aged;  allele;  article;  cell count;  cell population;  clinical trial;  controlled clinical trial;  controlled study;  female;  genetic polymorphism;  highly active antiretroviral therapy;  human;  Human immunodeficiency virus infection;  Kaplan Meier method;  major clinical study;  male;  priority journal;  prognosis;  T lymphocyte;  virus load, Acquired Immunodeficiency Syndrome;  Alleles;  Anti-HIV Agents;  Antiretroviral Therapy, Highly Active;  Chemokines, CXC;  HIV-1;  Humans;  Prognosis;  Receptors, Chemokine",
    abstract = "Background: The chemokine receptor polymorphisms CCR5Δ32, CXCL12 3′A, CCR2-64I and CCR5-59029 G/A have been demonstrated to affect HIV-1 infection and progression. Objective: We studied the impact of the above polymorphisms on the effectiveness of a 30-month treatment with highly active antiretroviral therapy (HAART) in 149 HIV-1 patients. Study design: We stratified the patients according to CD4 CDC criteria and applied Kaplan-Meier analysis using the following end-point criteria: (a) the time from HAART initiation to undetectable viral load (VL) counts (VL < 50 copies/ml), (b) the duration of undetectable VL status and (c) the time required for CD4+ T-cell counts to pass over the 500 cells/ml threshold. Results: Our results in the second group (CD4 201-500) revealed that patients with the CCR2-64I allele achieved undetectable VL counts at 3.5 ± 0.48 months as compared to 10.26 ± 1.42 months in the control group (p = 0.018). The VL remained undetectable for 28 ± 2 months, in contrast to 20 ± 2 months in the control group (p = 0.048). Patients carrying CXCL12 3′A restored the CD4 population faster than the control group (9 ± 2 and 14 ± 2 months, respectively, p = 0.023). The CCR5Δ32 and CCR5-59029 G/A alleles did not appear to affect the parameters studied. Conclusions: Our results suggest that patients carrying either CCR2-64I or CXCL12 3′A have a more favorable prognosis during HAART treatment. © 2005 Elsevier B.V. All rights reserved."
}