Background: Chemokines can block viral entry by interfering with HIV co-receptors and are recognised mediators\r\nof atherosclerosis development. A number of experimental drugs that inhibit HIV entry arrest the development of\r\natherosclerosis in animal models. We hypothesised that the expression of chemokine receptors in circulating\r\nleukocytes is associated with the rate of atherosclerosis progression in HIV-infected patients.\r\nMethods: The increase in intima-media thickness during a 2-year follow-up was used to classify HIV-infected\r\npatients (n = 178) as progressors (n = 142) or non-progressors (n = 36) with respect to atherosclerosis. Logistic\r\nregression was used to assess variables associated with atherosclerosis progression. Mutations in the CCR5?32,\r\nCCR2 64I, and CX3CR1 (T280M and V249I) co-receptors as well as the levels of CCR5, CXCR4, CX3CR1, and CCR2\r\nmRNA expression in circulating leukocytes were analysed as independent variables.\r\nResults: Among the baseline variables, only genetic variants explained the dichotomous outcome. The expression\r\nof CCR2 and CXCR4 did not discriminate between progressors and non-progressors. Conversely, CCR5 and CX3CR1\r\nexpression was higher in not only progressors but also patients with detectable viral load. The logistic regression,\r\nhowever, demonstrated a significant role for CCR5 expression as a predictor of atherosclerosis progression\r\n(B = 2.1, OR = 8.1, p = 0.04) and a negligible effect for CXC3R1 and CCR2 expression.\r\nConclusions: Available CCR5 antagonists should be investigated for their potential to delay the course of\r\natherosclerosis in HIV-infected patients.
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