HIV-1 adaptation to NK-cell-mediated immune pressure

Galit Alter, David Heckerman, Arne Schneidewind, Lena Fadda, Carl M. Kadie, Jonathan M. Carlson, Cesar Oniangue-Ndza, Maureen Martin, Bin Li, Salim I. Khakoo, Mary Carrington, Todd M. Allen and Marcus Altfeld ()
Additional contact information
Galit Alter: Ragon Institute at MGH, MIT and Harvard, Massachusetts General Hospital, Harvard Medical School
David Heckerman: Microsoft Research
Arne Schneidewind: Ragon Institute at MGH, MIT and Harvard, Massachusetts General Hospital, Harvard Medical School
Lena Fadda: Ragon Institute at MGH, MIT and Harvard, Massachusetts General Hospital, Harvard Medical School
Carl M. Kadie: Microsoft Research
Jonathan M. Carlson: Microsoft Research
Cesar Oniangue-Ndza: Ragon Institute at MGH, MIT and Harvard, Massachusetts General Hospital, Harvard Medical School
Maureen Martin: Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC Frederick Inc., NCI-Frederick, Frederick, Maryland 21702, USA
Bin Li: Ragon Institute at MGH, MIT and Harvard, Massachusetts General Hospital, Harvard Medical School
Salim I. Khakoo: Imperial College London, London W2 1PG, UK
Mary Carrington: Ragon Institute at MGH, MIT and Harvard, Massachusetts General Hospital, Harvard Medical School
Todd M. Allen: Ragon Institute at MGH, MIT and Harvard, Massachusetts General Hospital, Harvard Medical School
Marcus Altfeld: Ragon Institute at MGH, MIT and Harvard, Massachusetts General Hospital, Harvard Medical School

Nature, 2011, vol. 476, issue 7358, 96-100

Abstract: Natural killer cells and the control of HIV-1 Recent work has suggested that natural killer (NK) cells contribute to the control of HIV-1 infection through recognition of virally infected cells by both activating and inhibitory killer immunoglobulin-like receptors (KIRs). Alter et al. present evidence that NK cells select HIV escape mutants by an as-yet-undefined mechanism. This results in the inhibition of NK cell function, enabling HIV-1 to escape the potential protective role of this inhibitory KIR.

Date: 2011
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DOI: 10.1038/nature10237

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