Innate partnership of HLA-B and KIR3DL1 subtypes against HIV-1

Maureen P. Martin; Ying Qi; Xiaojiang Gao; Eriko Yamada; Jeffrey N. Martin; Florencia Pereyra; 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; Mary Carrington

doi:10.1038/ng2035

Innate partnership of HLA-B and KIR3DL1 subtypes against HIV-1

Maureen P. Martin, Ying Qi, Xiaojiang Gao, Eriko Yamada, Jeffrey N. Martin, Florencia Pereyra, 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. McVicarMary Carrington^*

^*Corresponding author for this work

Medicine, Infectious Diseases Division

Research output: Contribution to journal › Article › peer-review

593 Scopus citations

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.

Original language	English (US)
Pages (from-to)	733-740
Number of pages	8
Journal	Nature Genetics
Volume	39
Issue number	6
DOIs	https://doi.org/10.1038/ng2035
State	Published - Jun 2007

ASJC Scopus subject areas

Genetics

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/ng2035

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Martin, M. P., Qi, Y., Gao, X., Yamada, E., Martin, J. N., Pereyra, F., Colombo, S., Brown, E. E., Shupert, W. L., Phair, J., Goedert, J. J., Buchbinder, S., Kirk, G. D., Telenti, A., Connors, M., O'Brien, S. J., Walker, B. D., Parham, P., Deeks, S. G., ... Carrington, M. (2007). Innate partnership of HLA-B and KIR3DL1 subtypes against HIV-1. Nature Genetics, 39(6), 733-740. https://doi.org/10.1038/ng2035

@article{afcf566c87dc4023afd682a09de8a74e,

title = "Innate partnership of HLA-B and KIR3DL1 subtypes against HIV-1",

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.",

author = "Martin, {Maureen P.} and Ying Qi and Xiaojiang Gao and Eriko Yamada and Martin, {Jeffrey N.} and Florencia Pereyra and Sara Colombo and Brown, {Elizabeth E.} and Shupert, {W. Lesley} and John Phair and Goedert, {James J.} and Susan Buchbinder and Kirk, {Gregory D.} and Amalio Telenti and Mark Connors and O'Brien, {Stephen J.} and Walker, {Bruce D.} and Peter Parham and Deeks, {Steven G.} and McVicar, {Daniel W.} and Mary Carrington",

note = "Funding Information: This project has been funded in whole or in part with federal funds from the US National Cancer Institute, National Institutes of Health (NIH), under contract N01-CO-12400. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products or organizations imply endorsement by the US government. This research was supported in part by the Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research. The ALIVE study was supported by US National Institute on Drug Abuse RO1-DA04334. The SCOPE cohort was supported by the NIH (P30 AI027763) and the University of California at San Francisco AIDS Research Institute. The Swiss HIV Cohort study was funded by the Swiss National Science Foundation.",

year = "2007",

month = jun,

doi = "10.1038/ng2035",

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pages = "733--740",

journal = "Nature Genetics",

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Martin, MP, Qi, Y, Gao, X, Yamada, E, Martin, JN, Pereyra, F, Colombo, S, Brown, EE, Shupert, WL, Phair, J, Goedert, JJ, Buchbinder, S, Kirk, GD, Telenti, A, Connors, M, O'Brien, SJ, Walker, BD, Parham, P, Deeks, SG, McVicar, DW & Carrington, M 2007, 'Innate partnership of HLA-B and KIR3DL1 subtypes against HIV-1', Nature Genetics, vol. 39, no. 6, pp. 733-740. https://doi.org/10.1038/ng2035

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T1 - Innate partnership of HLA-B and KIR3DL1 subtypes against HIV-1

AU - Martin, Maureen P.

AU - Qi, Ying

AU - Gao, Xiaojiang

AU - Yamada, Eriko

AU - Martin, Jeffrey N.

AU - Pereyra, Florencia

AU - Colombo, Sara

AU - Brown, Elizabeth E.

AU - Shupert, W. Lesley

AU - Phair, John

AU - Goedert, James J.

AU - Buchbinder, Susan

AU - Kirk, Gregory D.

AU - Telenti, Amalio

AU - Connors, Mark

AU - O'Brien, Stephen J.

AU - Walker, Bruce D.

AU - Parham, Peter

AU - Deeks, Steven G.

AU - McVicar, Daniel W.

AU - Carrington, Mary

N1 - Funding Information: This project has been funded in whole or in part with federal funds from the US National Cancer Institute, National Institutes of Health (NIH), under contract N01-CO-12400. The content of this publication does not necessarily reflect the views or policies of the Department of Health and Human Services, nor does mention of trade names, commercial products or organizations imply endorsement by the US government. This research was supported in part by the Intramural Research Program of the NIH, National Cancer Institute, Center for Cancer Research. The ALIVE study was supported by US National Institute on Drug Abuse RO1-DA04334. The SCOPE cohort was supported by the NIH (P30 AI027763) and the University of California at San Francisco AIDS Research Institute. The Swiss HIV Cohort study was funded by the Swiss National Science Foundation.

PY - 2007/6

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N2 - 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.

AB - 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.

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JO - Nature Genetics

JF - Nature Genetics

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ER -

Innate partnership of HLA-B and KIR3DL1 subtypes against HIV-1

Abstract

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