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Journal of Virology, July 2009, p. 6798-6805, Vol. 83, No. 13
0022-538X/09/$08.00+0 doi:10.1128/JVI.00256-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Eric S. Rosenberg,1
Jeffrey S. Miller,3
Mary Carrington,2,
and
Marcus Altfeld1
Ragon Institute of MGH, MIT, and Harvard; Infectious Disease Unit, Massachusetts General Hospital; and Division of AIDS, Harvard Medical School, Boston, Massachusetts,1 Basic Research Program, SAIC-Frederick, Inc., Laboratory of Genomic Diversity, Frederick, Maryland,2 Division of Hematology, Oncology and Transplantation, University of Minnesota Cancer Center, Minneapolis, Minnesota3
Received 5 February 2009/ Accepted 13 April 2009
NK cells are critical in the early containment of viral infections. Epidemiological and functional studies have shown an important role of NK cells expressing specific killer immunoglobulin-like receptors (KIRs) in the control of human immunodeficiency virus type 1 (HIV-1) infection, but little is known about the mechanisms that determine the expansion of these antiviral NK cell populations during acute HIV-1 infection. Here we demonstrate that NK cells expressing the activating receptor KIR3DS1+ and, to a lesser extent, the inhibitory receptor KIR3DL1+ specifically expand in acute HIV-1 infection in the presence of HLA-B Bw480I, the putative HLA class I ligand for KIR3DL1/3DS1. These data demonstrate for the first time the HLA class I subtype-dependent expansion of specific KIR+ NK cells during an acute viral infection in humans.
Published ahead of print on 22 April 2009.
Present address: Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC-Frederick, Inc., NCI-Frederick, Frederick, MD.
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