Abstract
While the contribution of CD8+ cytotoxic T lymphocytes to early containment of HIV-1 spread is well established, a role for NK cells in controlling HIV-1 replication during primary infection has been uncertain. The highly polymorphic family of KIR molecules expressed on NK cells can inhibit or activate these effector cells and might therefore modulate their activity against HIV-1-infected cells. In the present study, we investigated copy number variation in KIR3DH loci encoding the only activating KIR receptor family in rhesus monkeys and its effect on simian immunodeficiency virus (SIV) replication during primary infection in rhesus monkeys. We observed an association between copy numbers of KIR3DH genes and control of SIV replication in Mamu-A*01– rhesus monkeys that express restrictive TRIM5 alleles. These findings provide further evidence for an association between NK cells and the early containment of SIV replication, and underscore the potential importance of activating KIRs in stimulating NK cell responses to control SIV spread.
Highlights
Natural killer (NK) cells are the primary effector cells of the innate immune system, representing a first line of defense against viruses through their ability to lyse virally infected cells without prior antigen sensitization [1,2,3]
This study was initiated to explore the copy number variation of activating killer cell immunoglobulin-like receptors (KIR) genes of Indian-origin rhesus monkeys and its NK cells are effector cells of the innate immune system that contribute to protection against virus infections through their ability to lyse virus-infected cells without prior antigen sensitization
We identify an association between the copy number of activating KIR genes in rhesus monkeys and the control of simian immunodeficiency virus (SIV) replication during primary infection in Mamu-A*01– rhesus monkeys that express restrictive TRIM5 alleles
Summary
Natural killer (NK) cells are the primary effector cells of the innate immune system, representing a first line of defense against viruses through their ability to lyse virally infected cells without prior antigen sensitization [1,2,3]. Inhibitory receptors transmit inhibitory signals to NK cells that protect healthy cells from destruction by NK cell-mediated cytotoxicity, whereas activating NK cell receptors transmit activating signals to these effector cells It is the balance of these opposing signals that determines the activation state of an NK cell and, in so doing, regulates NK cell-mediated killing and cytokine production [5,6,7]. Among these receptor families expressed by NK cells are the inhibitory and activating killer cell immunoglobulin-like receptors (KIR). The highly polymorphic KIRs recognize MHC class I molecules as ligands [8,9], and the coincident expression of certain KIRs and MHC class I molecules in an individual influences the outcome of a number of viral infections [10,11]
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