Chemokine receptor genetic mutations are among the factors which have been shown to influence human susceptibility to HIV-1 infection and progression. The CCR2-64I mutation has been shown to delay HIV-1 disease progression in some studies. Here we show evidence of delayed disease progression, reflected in maintenance of a stable viral load and a slow CD4 T-cell decline, in a patient with the CCR2-64I gene. We then consider the potential value of identifying these genetic defects in the era of fusion/entry inhibiting therapeutics.
Rapid CD4+ T-cell decline is associated with coreceptor switch among MSM primarily infected with HIV-1 CRF01_AE in Northeast China