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: CCR5͞CCR5 (homozygous, wild type), CCR5͞CCR5⌬32 (heterozygous), and CCR5⌬32͞CCR5⌬32 (homozygous, mutant). Our results indicate that prevalence of HIV͞ 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.