Send to

Choose Destination
See comment in PubMed Commons below
Proc Natl Acad Sci U S A. 2001 Aug 28;98(18):10214-9. Epub 2001 Aug 21.

The coreceptor mutation CCR5Delta32 influences the dynamics of HIV epidemics and is selected for by HIV.

Author information

  • 1Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI 48109-0620, USA.


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, CCR5Delta32. Individuals homozygous for CCR5Delta32 are protected against HIV infection whereas those heterozygous for CCR5Delta32 have lower pre-AIDS viral loads and delayed progression to AIDS. CCR5Delta32 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/CCR5Delta32 (heterozygous), and CCR5Delta32/CCR5Delta32 (homozygous, mutant). Our results indicate that prevalence of HIV/AIDS is greater in populations lacking the CCR5Delta32 alleles (homozygous wild types only) as compared with populations that include people heterozygous or homozygous for CCR5Delta32. Also, we show that HIV can provide selective pressure for CCR5Delta32, increasing the frequency of this allele.

[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center