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Understanding why some people establish and maintain effective control of HIV-1 and others do not is a priority in the effort to develop new treatments for HIV/AIDS. Using a whole-genome association strategy, we identified polymorphisms that explain nearly 15% of the variation among individuals in viral load during the asymptomatic set-point period of infection. One of these is found within an endogenous retroviral element and is associated with major histocompatibility allele human leukocyte antigen (HLA)-B*5701, whereas a second is located near the HLA-C gene. An additional analysis of the time to HIV disease progression implicated two genes, one of which encodes an RNA polymerase I subunit. These findings emphasize the importance of studying human genetic variation as a guide to combating infectious agents.

Original publication

DOI

10.1126/science.1143767

Type

Journal article

Journal

Science

Publication Date

17/08/2007

Volume

317

Pages

944 - 947

Keywords

Cohort Studies, DNA-Binding Proteins, Disease Progression, Female, Genes, MHC Class I, Genome, Human, HIV Infections, HIV-1, HLA-B Antigens, HLA-C Antigens, Haplotypes, Humans, Immediate-Early Proteins, Major Histocompatibility Complex, Male, Polymorphism, Single Nucleotide, RNA, Long Noncoding, RNA, Untranslated, Regression Analysis, Viral Load