The coreceptor mutation CCR5Δ32 influences the dynamics of HIV epidemics and is selected for by HIV

We explore the impact of a host genetic factor on heterosexual HIV epidemics by using a deterministic mathematical model. A protective allele unequally distributed across populations is exemplified in our models by the 32-bp deletion in the host-cell chemokine receptor CCR5, CCR5 Delta 32. Individuals homozygous for CCR5 Delta 32 are protected against HIV infection whereas those heterozygous for CCR5A32 have lower pre-AIDS viral loads and delayed progression to AIDS. CCR5A32 may limit HIV spread by decreasing the probability of both risk of infection and infectiousness. In this work, we characterize epidemic HIV within three dynamic subpopulations: CCR5/CCR5 (homozygous, wild type), CCR5/CCR5 Delta 32 (heterozygous), and CCR5 Delta 32/CCR5 Delta 32 (homozygous, mutant). Our results indicate that prevalence of HIV/ AIDS is greater in populations lacking the CCR5A32 alleles (homozygous wild types only) as compared with populations that include people heterozygous or homozygous for CCR5 Delta 32. Also, we show that HIV can provide selective pressure for CCR5 Delta 32, increasing the frequency of this allele.