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I ndividual susceptibility to infectious disease, such as HIV-1, is strongly influenced by the genetic profile of the host. Allelic variants of the human major histocompatibility complex (human leukocyte antigen [HLA]) genes have been implicated repeatedly with susceptibility, course, and outcome of HIV-1 infection [1]. The HLA Class I loci is genetically diverse, and in addition to its functions in presenting peptide fragments of the invading pathogen to CD8þ T cells, may assume other functions, such as direct interaction with natural killer (NK) cells. Alleles of the Class I A and B loci form the Bw4/Bw6 cluster, a grouping based on an exposed epitope on the a1 helix, on the lip of the peptide binding cleft. This region of the HLA molecule is known to interact with NK cells via the killer Ig-like receptor (KIR). Expressed on the NK cell surface, KIR is allelic, with forms that, upon engagement with an HLA Class I ligand, may either inhibit or activate an NK cell. The KIR receptor alleles fall into two broad groups: forms with a long cytoplasmic tail (such as KIR2DL1) bear an immune tyrosine inhibitory motif and inhibit, while the short-tail forms (such as KIR2DS2) activate NK cells [2]. Upon engagement with an HLA Class I ligand, short-tail forms of KIR may increase NK cell effector activity, inducing the release of perforin and granzyme, and secretion of IFN-c [2] .

Correction: Synergy or Independence? Deciphering the Interaction of HLA Class I and NK Cell KIR Alleles in Early HIV-1 Disease Progression