Biology Faculty Articles
Title
Innate Partnership of HLA-B and KIR3DL1 Subtypes Against HIV-1
Document Type
Article
Publication Date
6-2007
Publication Title
Nature Genetics
ISSN
1061-4036
Volume
39
Issue/No.
6
First Page
733
Last Page
740
Abstract
Allotypes of the natural killer (NK) cell receptor KIR3DL1 vary in both NK cell expression patterns and inhibitory capacity upon binding to their ligands, HLA-B Bw4 molecules, present on target cells. Using a sample size of over 1,500 human immunodeficiency virus (HIV)+ individuals, we show that various distinct allelic combinations of the KIR3DL1 and HLA-B loci significantly and strongly influence both AIDS progression and plasma HIV RNA abundance in a consistent manner. These genetic data correlate very well with previously defined functional differences that distinguish KIR3DL1 allotypes. The various epistatic effects observed here for common, distinct KIR3DL1 and HLA-B Bw4 combinations are unprecedented with regard to any pair of genetic loci in human disease, and indicate that NK cells may have a critical role in the natural history of HIV infection.
Additional Comments
National Cancer Institute contract #: N01-CO-12400; US National Institute on Drug Abuse grant #: RO1-DA04334; NIH grant #: P30 AI027763
NSUWorks Citation
Martin, Maureen P.; Ying Qi; Xiaojiang Gao; Eriko Yamada; Jeffrey N. Martin; Florencia Fereyra; Sara Colombo; Elizabeth E. Brown; W. Lesley Shupert; John Phair; James J. Goedert; Susan Buchbinder; Gregory D. Kirk; Amalio Telenti; Mark Connors; Stephen J. O'Brien; Bruce D. Walker; Peter Parham; Steven G. Deeks; Daniel W. McVicar; and Mary Carrington. 2007. "Innate Partnership of HLA-B and KIR3DL1 Subtypes Against HIV-1." Nature Genetics 39, (6): 733-740. https://nsuworks.nova.edu/cnso_bio_facarticles/507
ORCID ID
0000-0001-7353-8301
ResearcherID
N-1726-2015
Comments
©2007 Nature Publishing Group