Multiple KIR gene polymorphisms are associated with plasma viral loads in SIV-infected rhesus macaques

• Type of Material: Article
• Authors: Porntip Chaichompoo, Emory University; Pavel Bostik, Emory University; Susan Stephenson, Emory University; Suthiphol Udompunturuk, Mahidol University; Jaruda Kobkitjaroen, Mahidol University; Kovit Pattanapanyasat, Mahidol University; Aftab A Ansari, Emory University
• Language: English
• Date: 2010
• Publisher: Elsevier
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2010 Elsevier Inc. All rights reserved
• License: Creative Commons Attribution-NonCommerical-NoDerivs 3.0 Unported
• Final Published Version (URL): http://dx.doi.org/10.1016/j.cellimm.2010.03.014
• Title of Journal or Parent Work: Cellular Immunology
• ISSN: 0008-8749
• Volume: 263
• Issue: 2
• Start Page: 176
• End Page: 187
• Grant/Funding Information: Supported by NIH NIAID RO1 AI078773, NIH-NCRR-DRR base grant 000165 to the Yerkes National Primate Research Center, the Thailand Research Fund – Senior Research Scholar and Royal Golden Jubilee and the Grant Agency of the Czech Republic, grant no. P304-10-1161.
• Keywords: nonhuman primates; polymorphisms; Innate immunity; genetics; viral loads; NK cells; MHC; SIV; KIR's; rhesus macaques
• Research Categories: Health Sciences, Pathology; Health Sciences, Immunology

Abstract

Innate immune mechanisms play a deterministic role in the rate of disease progression during acute infection in HIV infected humans and SIV infection of nonhuman primates. The role NK cells play in mediating such an effect has thus gained importance. One of the major sets of molecules that regulate NK cell function are the killer cell immunoglobulin like molecules (KIR's). Our laboratory has previously shown an association of KIR3DL alleles 13–14 with high plasma viral loads in a cohort of SIV infected rhesus macaques. To gain a more detailed understanding of the role of KIR polymorphisms, our laboratory herein conducted studies of 3 additional KIR loci and show that select KIR3DH alleles appear to be more strongly associated with high plasma viral loads than KIR3DL alleles 13–14. In addition, we herein document the existence of additional new alleles for the KIR1D, KIR2DL4, and the KIR3DH loci.