Additive Contribution of HLA Class I Alleles in the Immune Control of HIV-1 Infection


Por: Leslie, A, Matthews, PC, Listgarten, J, Carlson, JM, Kadie, C, Ndung'u, T, Brander, C, Coovadia, H, Walker, BD, Heckerman, D and Goulder, PJR

Publicada: 1 oct 2010
Resumen:
Previous studies have identified a central role for HLA-B alleles in influencing control of HIV infection. An alternative possibility is that a small number of HLA-B alleles may have a very strong impact on HIV disease outcome, dominating the contribution of other HLA alleles. Here, we find that even following the exclusion of subjects expressing any of the HLA-B class I alleles (B*57, B*58, and B*18) identified to have the strongest influence on control, the dominant impact of HLA-B alleles on virus set point and absolute CD4 count variation remains significant. However, we also find that the influence of HLA on HIV control in this C-clade-infected cohort from South Africa extends beyond HLA-B as HLA-Cw type remains a significant predictor of virus and CD4 count following exclusion of the strongest HLA-B associations. Furthermore, there is evidence of interdependent protective effects of the HLA-Cw*0401-B*8101, HLA-Cw*1203-B*3910, and HLA-A*7401-B*5703 haplotypes that cannot be explained solely by linkage to a protective HLA-B allele. Analysis of individuals expressing both protective and detrimental alleles shows that even the strongest HLA alleles appear to have an additive rather than dominant effect on HIV control at the individual level. Finally, weak but significant frequency-dependent effects in this cohort can be detected only by looking at an individual's combined HLA allele frequencies. Taken together, these data suggest that although individual HLA alleles, particularly HLA-B, can have a strong impact, HIV control overall is likely to be influenced by the additive effect of some or all of the other HLA alleles present.

Filiaciones:
Leslie, A:
 Univ Oxford, Weatherall Inst Mol Med, Oxford OX1 3SY, England

Matthews, PC:
 Univ Oxford, Nuffield Dept Med, Dept Paediat, Oxford OX1 3SY, England

Listgarten, J:
 Microsoft Res, Machine Learning & Appl Stat Grp, Redmond, WA USA

Carlson, JM:
 Microsoft Res, Machine Learning & Appl Stat Grp, Redmond, WA USA

Kadie, C:
 Microsoft Res, Machine Learning & Appl Stat Grp, Redmond, WA USA

Ndung'u, T:
 Univ KwaZulu Natal, Doris Duke Med Res Inst, HIV Pathogenesis Programme, Durban, South Africa

:
 Hosp Badalona Germans Trias & Pujol, Fundacio IrsiCaixa HIVACAT, Badalona, Spain

 Inst Catalana Recerca & Estudis Avancats, Barcelona 08916, Spain

Coovadia, H:
 Univ KwaZulu Natal, Doris Duke Med Res Inst, HIV Pathogenesis Programme, Durban, South Africa

Walker, BD:
 Univ KwaZulu Natal, Doris Duke Med Res Inst, HIV Pathogenesis Programme, Durban, South Africa

 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ragon Inst, Boston, MA USA

 Howard Hughes Med Inst, Chevy Chase, MD USA

Heckerman, D:
 Microsoft Res, Machine Learning & Appl Stat Grp, Redmond, WA USA

Goulder, PJR:
 Univ Oxford, Nuffield Dept Med, Dept Paediat, Oxford OX1 3SY, England

 Univ KwaZulu Natal, Doris Duke Med Res Inst, HIV Pathogenesis Programme, Durban, South Africa

 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ragon Inst, Boston, MA USA
ISSN: 10985514





Journal of Virology
Editorial
American Society for Microbiology, 1752 N ST NW, WASHINGTON, DC 20036-2904 USA, Estados Unidos America
Tipo de documento: Article
Volumen: 84 Número: 19
Páginas: 9879-9888
WOS Id: 000282641800021
ID de PubMed: 20660184
imagen Green Published

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