期刊
SCIENCE
卷 317, 期 5840, 页码 944-947出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1143767
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资金
- MRC [MC_U137884177, G0200585] Funding Source: UKRI
- Medical Research Council [MC_U137884177, G0200585] Funding Source: researchfish
- ICREA Funding Source: Custom
- Medical Research Council [MC_U137884177, G0200585] Funding Source: Medline
- NIAID NIH HHS [U19 AI067854, U19 AI067854-03] Funding Source: Medline
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.
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