Polymorphisms of Cx3CR1 and CXCR6 receptors in relation to HAART therapy of HIV type 1 patients

The chemokine polymorphisms CXCR6-3E/K, In1.1T/C, H7 haplotype, CX 3CR1-V249I, and CX3CR1-T280M have been shown to affect the course of HIV infection. We studied their influence on immunologic and virologic response to HAART in a group of 143 HIV-1 patients. We performed Kaplan-Meier analysis using the following end-point criteria: (1) time from HAART initiation to undetectable viral load (VL < 50 copies/ml), (2) maximum duration of viral suppression, (3) time from HAART administration until CD4 elevation above 200 cells/μl for patients with baseline CD4 below 200 cells/μl and above 500 cells/μl for patients with baseline CD4 between 200 and 500 cells/μl, respectively, and (4) time from HAART initiation until CD4 reduction below baseline values. Our results revealed an improved immunologic response to HAART in patients with the CX3CR1-249I or CX 3CR1-280M allele. On the contrary, patients with initial VL suppression due to HAART showed a faster virologic failure in the presence of the CXCR6-3K allele. The In1.1T/C polymorphism and H7 haplotype did not reveal any specific effect on HAART response. © Mary Ann Liebert, Inc

CCR2-64I and CXCL12 3′A alleles confer a favorable prognosis to AIDS patients undergoing HAART therapy

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

Polymorphisms of Cx(3)CR1 and CXCR6 receptors in relation to HAART therapy of HIV type 1 patients

The chemokine polymorphisms CXCR6-3E/K, In1.1T/C, H7 haplotype, CX(3)CR1-V249I, and CX(3)CR1-T280M have been shown to affect the course of HIV infection. We studied their influence on immunologic and virologic response to HAART in a group of 143 HIV-1 patients. We performed Kaplan-Meier analysis using the following end-point criteria: (1) time from HAART initiation to undetectable viral load (VL < 50 copies/ml), (2) maximum duration of viral suppression, (3) time from HAART administration until CD4 elevation above 200 cells/mu l for patients with baseline CD4 below 200 cells/mu l and above 500 cells/mu l for patients with baseline CD4 between 200 and 500 cells/mu l, respectively, and (4) time from HAART initiation until CD4 reduction below baseline values. Our results revealed an improved immunologic response to HAART in patients with the CX(3)CR1-249I or CX(3)CR1-280M allele. On the contrary, patients with initial VL suppression due to HAART showed a faster virologic failure in the presence of the CXCR6-3K allele. The In1.1T/C polymorphism and H7 haplotype did not reveal any specific effect on HAART response