Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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




Journal article



Publication Date





944 - 947


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