Biology Faculty Articles
Title
Haplotype Diversity in the Interleukin-4 Gene is Not Associated with HIV-1 transmission and AIDS Progression
Document Type
Article
Publication Date
6-2003
Publication Title
Immunogenetics
Keywords
HIV-1, AIDS, Interleukin-4, Haplotype diversity, Recombination hotspot
ISSN
0093-7711
Volume
55
Issue/No.
3
First Page
157
Last Page
164
Abstract
Interleukin-4 (IL-4) is a pleiotropic cytokine produced primarily by activated CD4+ T lymphocytes, mast cells, and basophils. It modulates the functions of a variety of cell types involved with the immune response. This cytokine differentially regulates two major HIV-1 coreceptors and activates viral expression, and is thus a reasonable candidate gene for analyses in HIV-1/AIDS cohort studies. Population genetic variation in five single nucleotide polymorphisms (SNPs) in the 5′ region of the IL-4 gene was assessed in five racial groups. Neutrality tests reveal that the populations are evolving in accord with the infinite-sites model. However, coalescent simulations suggest greater haplotype diversity among African Americans than expected. This increased variation is presumably attributable to recombination or gene conversion. Genetic epidemiological analyses were conducted among European American and African American participants enrolled in five USA-based HIV-1/AIDS cohorts. One SNP, −589T, known to influence IL-4 transcription was previously shown to be associated with HIV-1/AIDS in both Japanese and French populations. Present analyses failed to identify any significant associations with HIV-1 infection or progression to AIDS.
Additional Comments
National Cancer Institute contract #: NO1-CO-124000
NSUWorks Citation
Modi, William; Thomas R. O'Brien; David Vlahov; Susan Buchbinder; Edward Gomperts; John Phair; Stephen J. O'Brien; and Cheryl Winkler. 2003. "Haplotype Diversity in the Interleukin-4 Gene is Not Associated with HIV-1 transmission and AIDS Progression." Immunogenetics 55, (3): 157-164. https://nsuworks.nova.edu/cnso_bio_facarticles/589
ORCID ID
0000-0001-7353-8301
ResearcherID
N-1726-2015
Comments
©Springer-Verlag 2003