%0 Journal Article %1 sullivan_coreceptor_2001 %A Sullivan, A D %A Wigginton, J %A Kirschner, D %D 2001 %J Proceedings of the National Academy of Sciences of the United States of America %K Alleles, Biological, Disease Female, Frequency, Gene Heterosexuality, Heterozygote, Homozygote, Humans, Infections, Male, Models, Mutation, Outbreaks, Receptors, Selection {(Genetics)} {CCR5,} {HIV,} {HIV} %N 18 %P 10214--10219 %R 10.1073/pnas.181325198 %T The coreceptor mutation CCR5Delta32 influences the dynamics of HIV epidemics and is selected for by HIV %U http://www.ncbi.nlm.nih.gov/pubmed/11517319 %V 98 %X 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.

@article{sullivan_coreceptor_2001, abstract = {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.}, added-at = {2011-03-11T10:05:34.000+0100}, author = {Sullivan, A D and Wigginton, J and Kirschner, D}, biburl = {https://www.bibsonomy.org/bibtex/2b8565848d81d5f632b82b4522872e457/jelias}, doi = {10.1073/pnas.181325198}, interhash = {a743b9f1356951cd253094f787683a36}, intrahash = {b8565848d81d5f632b82b4522872e457}, issn = {0027-8424}, journal = {Proceedings of the National Academy of Sciences of the United States of America}, keywords = {Alleles, Biological, Disease Female, Frequency, Gene Heterosexuality, Heterozygote, Homozygote, Humans, Infections, Male, Models, Mutation, Outbreaks, Receptors, Selection {(Genetics)} {CCR5,} {HIV,} {HIV}}, month = aug, note = {{PMID:} 11517319}, number = 18, pages = {10214--10219}, timestamp = {2011-03-11T10:05:56.000+0100}, title = {The coreceptor mutation {CCR5Delta32} influences the dynamics of {HIV} epidemics and is selected for by {HIV}}, url = {http://www.ncbi.nlm.nih.gov/pubmed/11517319}, volume = 98, year = 2001 }