Innate Partnership of HLA-B and KIR3DL1 Subtypes Against HIV-1

Authors

• Maureen P. Martin, National Cancer Institute at Frederick
• Ying Qi, National Cancer Institute at Frederick
• Xiaojiang Gao, National Cancer Institute at Frederick
• Eriko Yamada, National Cancer Institute at Frederick
• Jeffrey N. Martin, University of California - San Francisco
• Florencia Fereyra, Harvard Medical School
• Sara Colombo, University of Lausanne - Switzerland
• Elizabeth E. Brown, National Cancer Institute at Rockville
• W. Lesley Shupert, National Institute of Allergy and Infectious Diseases
• John Phair, Northwestern University Medical School
• James J. Goedert, National Cancer Institute at Rockville
• Susan Buchbinder, San Francisco Department of Public Health
• Gregory D. Kirk, Johns Hopkins University
• Amalio Telenti, University of Lausanne - Switzerland
• Mark Connors, National Institute of Allergy and Infectious Diseases
• Stephen J. O'Brien, National Cancer Institute at FrederickFollow
• Bruce D. Walker, Harvard Medical School
• Peter Parham, Stanford University
• Steven G. Deeks, San Francisco General Hospital
• Daniel W. McVicar, National Cancer Institute at Frederick
• Mary Carrington, National Cancer Institute at Frederick

ORCID

0000-0001-7353-8301

ResearcherID

N-1726-2015

Document Type

Article

Publication Title

Nature Genetics

ISSN

1061-4036

Publication Date

6-2007

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.

Volume

39

Issue

6

First Page

733

Last Page

740

Comments

©2007 Nature Publishing Group

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