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Killer immunoglobulin-like receptors and HLA act both independently and synergistically to modify HIV disease progression.

Gaudieri S, DeSantis D, McKinnon E, Moore C, Nolan D, Witt CS, Mallal SA, Christiansen FT

Centre for Clinical Immunology and Biomedical Statistics, Murdoch University and Royal Perth Hospital, Wellington Street, Perth, Western Australia 6000, Australia.

Variation in the host response to infection by pathogens including HIV-1 may be conferred by polymorphic genetic factors such as HLA and killer immunoglobulin-like receptors (KIR) genes. Here, we examined KIR and HLA genotype effects on pretreatment viral load, rate of CD4(+) T-cell decline and progression to AIDS among adult HIV-1-infected patients within the Western Australian HIV Study Cohort. In this study, carriage of KIR genes within the 'B' haplotype (eg KIR2DS2) was specifically associated with a more rapid CD4(+) T-cell decline over time and progression to AIDS. In contrast, KIR gene repertoire had no effect on pretreatment viral load while selected HLA alleles (eg HLA-B*5701, HLA-B*2705) demonstrated significant protective effects on viremia. Furthermore, interactions between specific HLA and KIR genes did appear to influence HIV disease progression. The results suggest that host genetic variation within the HLA and KIR gene complexes have clinically relevant effects on the course of HIV-1/AIDS, acting independently as well as synergistically to modify disease progression at multiple levels.

Published 1 December 2005 in Genes Immun, 6(8): 683-90.
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