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∆32. Individuals homozygous for CCR5∆32 are protected against HIV infection whereas those heterozygous for CCR5∆32 have lower pre-AIDS viral loads and delayed progression to AIDS. CCR5∆32 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∆32 (heterozygous), and CCR5∆32/CCR5∆32 (homozygous, mutant). Our results indicate that prevalence of HIV/AIDS is greater in populations lacking the CCR5∆32 alleles (homozygous wild types only) as compared with populations that include people heterozygous or homozygous for CCR5∆32. Also, we show that HIV can provide selective pressure for CCR5∆32, increasing the frequency of this allele.