Journal
NATURE GENETICS
Volume 41, Issue 12, Pages 1290-U46Publisher
NATURE PORTFOLIO
DOI: 10.1038/ng.486
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Funding
- National Cancer Institute, National Institutes of Health [HHSN261200800001E, N02-CP-55504, R01-DA04334, R01-DA12568]
- Intramural Research Program of the NIH
- National Cancer Institute, Center for Cancer Research
- Bill & Melinda Gates Foundation
- Swiss National Science Foundation
- SCOPE
- Clinical and Translational Sciences Award [UL1 RR024131]
- Center for AIDS Research [P30 AI27763]
- Cambridge Center for Trophoblast Research
- NATIONAL CANCER INSTITUTE [ZIABC010747, ZICBC011237, ZIABC010791] Funding Source: NIH RePORTER
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A variant 35 kb upstream of the HLA-C gene (-35C/T) was previously shown to associate with HLA-C mRNA expression level and steady-state plasma HIV RNA levels. We genotyped this variant in 1,698 patients of European ancestry with HIV. Individuals with known seroconversion dates were used for disease progression analysis and those with longitudinal viral load data were used for viral load analysis. We further tested cell surface expression of HLA-C in normal donors using an HLA-C-specific antibody. We show that the -35C allele is a proxy for high HLA-C cell surface expression, and that individuals with high-expressing HLA-C alleles progress more slowly to AIDS and control viremia significantly better than individuals with low HLA-C expressing alleles. These data strongly implicate high HLA-C expression levels in more effective control of HIV-1, potentially through better antigen presentation to cytotoxic T lymphocytes or recognition and killing of infected cells by natural killer cells.
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