BACKGROUND AND PURPOSE: The initial steps of atherosclerosis and the entry of HIV into the cell share similar biological mechanisms. Therefore, our hypothesis is that the progression of atherosclerosis in patients with HIV infection can be influenced by variations in genes implicated in both processes. METHODS: The progression of atherosclerosis over a 2-year follow-up period was measured as the combined carotid and femoral intima media thickness (IMT) in 141 patients with HIV infection. The DeltaIMT (IMT(follow-up)-IMT(baseline)) values were used to segregate patients as minimal progressors or regressors (lowest DeltaIMT tertile), slow progressors (mid DeltaIMT tertile), and rapid progressors (highest DeltaIMT tertile). Mutations CCR-5Delta32, CCR-2 64I, MCP-1-2518G, SDF1-3'A, and CX3CR-1 (T280 mol/L and V249I) in the host DNA were determined. Mean age of the patients was 38.96 (SEM: 0.61) and 68.8% were male. The mean DeltaIMT was 0.045 mm (0.01) per year, which represented a significant progression (P<0.001) with respect to baseline values. Patients with minimal progression or regression had a significantly (P=0.01) higher CD4 cell count than slow progressors and rapid progressors. Multivariate analyses indicated that age and total cholesterol were positively associated with IMT progression. In contrast, the CD4 cell count, the SDF1-3'A, and the CX3CR-1 249 I mutated alleles were associated with lesser IMT progression. CONCLUSIONS: The course of atherosclerosis in patients with HIV infection is influenced by polymorphisms in the SDF1 and CX3CR1 genes by metabolic variables and by the CD4 cell count. These data would be of help in assessing therapeutic needs of these patients.
BACKGROUND AND PURPOSE: The initial steps of atherosclerosis and the entry of HIV into the cell share similar biological mechanisms. Therefore, our hypothesis is that the progression of atherosclerosis in patients with HIV infection can be influenced by variations in genes implicated in both processes. METHODS: The progression of atherosclerosis over a 2-year follow-up period was measured as the combined carotid and femoral intima media thickness (IMT) in 141 patients with HIV infection. The DeltaIMT (IMT(follow-up)-IMT(baseline)) values were used to segregate patients as minimal progressors or regressors (lowest DeltaIMT tertile), slow progressors (mid DeltaIMT tertile), and rapid progressors (highest DeltaIMT tertile). Mutations CCR-5Delta32, CCR-2 64I, MCP-1-2518G, SDF1-3'A, and CX3CR-1 (T280 mol/L and V249I) in the host DNA were determined. Mean age of the patients was 38.96 (SEM: 0.61) and 68.8% were male. The mean DeltaIMT was 0.045 mm (0.01) per year, which represented a significant progression (P<0.001) with respect to baseline values. Patients with minimal progression or regression had a significantly (P=0.01) higher CD4 cell count than slow progressors and rapid progressors. Multivariate analyses indicated that age and total cholesterol were positively associated with IMT progression. In contrast, the CD4 cell count, the SDF1-3'A, and the CX3CR-1 249 I mutated alleles were associated with lesser IMT progression. CONCLUSIONS: The course of atherosclerosis in patients with HIV infection is influenced by polymorphisms in the SDF1 and CX3CR1 genes by metabolic variables and by the CD4 cell count. These data would be of help in assessing therapeutic needs of these patients.
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