The Journal of Experimental Medicine
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Published online
doi:10.1084/jem.20070695
The Journal of Experimental Medicine, Vol. 204, No. 12, 3027-3036
The Rockefeller University Press, 0022-1007 $30.00
© Alter et al.
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ARTICLE

 Differential natural killer cell–mediated inhibition of HIV-1 replication based on distinct KIR/HLA subtypes

Galit Alter1, Maureen P. Martin2, Nickolas Teigen1, William H. Carr1, Todd J. Suscovich1, Arne Schneidewind1, Hendrik Streeck1, Michael Waring1, Angela Meier1, Christian Brander1, Jeffrey D. Lifson3, Todd M. Allen1, Mary Carrington2, and Marcus Altfeld1

1 Partners AIDS Research Center and Infectious Disease Unit, Massachusetts General Hospital and Division of AIDS, Harvard Medical School, Boston, MA 02129
2 Laboratory of Genomic Diversity and 3 Retroviral Pathogenesis Section, Basic Research Program, SAIC-Frederick, Inc., Frederick, MD 21702

CORRESPONDENCE Marcus Altfeld: maltfeld{at}partners.org

Decline of peak viremia during acute HIV-1 infection occurs before the development of vigorous adaptive immunity, and the level of decline correlates inversely with the rate of AIDS progression, implicating a potential role for the innate immune response in determining disease outcome. The combined expression of an activating natural killer (NK) cell receptor, the killer immunoglobulin-like receptor (KIR) 3DS1, and its presumed ligand, human leukocyte antigen (HLA)–B Bw4-80I, has been associated in epidemiological studies with a slow progression to AIDS. We examined the functional ability of NK cells to differentially control HIV-1 replication in vitro based on their KIR and HLA types. NK cells expressing KIR3DS1 showed strong, significant dose- and cell contact–dependent inhibition of HIV-1 replication in target cells expressing HLA-B Bw4-80I compared with NK cells that did not express KIR3DS1. Furthermore, KIR3DS1+ NK cells and NKLs were preferentially activated, and lysed HIV-1 infected target cells in an HLA-B Bw4-80I–dependent manner. These data provide the first functional evidence that variation at the KIR locus influences the effectiveness of NK cell activity in the containment of viral replication.

Abbreviations used: CCR, CC chemokine receptor; E/T, effector/target; HLA, human leukocyte antigen; KIR, killer immunoglobulin-like receptor; MFI, mean fluorescence intensity; SSO, thianthrene 5-oxide.


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