The clinical course of HIV-1 infection can be highly variable between individuals. The period of asymptomatic disease after HIV-1 infection in the absence of antiviral therapy is typically 7–11 years [1], [2], with extremes of disease progression within 2 years, or virtually no disease progression for more than 15 years [3]. The genetic make-up of an individual has been shown to play a role in the susceptibility to HIV-1 infection and/or the rate of disease progression. Some of the observed variation could be attributed to human leukocyte antigen (HLA) types. In the Caucasian population, HLA-B5701 and HLA-B27 are most strongly associated with prolonged survival, whereas a variant of HLA-B35 is linked to an accelerated progression to AIDS [4]–[7]. Another well known example is the 32 base pair deletion in the gene coding for the chemokine receptor CCR5 that serves as a coreceptor for HIV-1. This polymorphism has been associated with reduced susceptibility to infection [8], [9] and a slower rate of disease progression [10]–[12]. However, all host genetic factors identified to date can explain the clinical course of HIV-1 infection in only a minority of individuals [13], [14].
