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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2004-3-1
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pubmed:abstractText |
Within-patient HIV evolution reflects the strong selection pressure driving viral escape from cytotoxic T-lymphocyte (CTL) recognition. Whether this intrapatient accumulation of escape mutations translates into HIV evolution at the population level has not been evaluated. We studied over 300 patients drawn from the B- and C-clade epidemics, focusing on human leukocyte antigen (HLA) alleles HLA-B57 and HLA-B5801, which are associated with long-term HIV control and are therefore likely to exert strong selection pressure on the virus. The CTL response dominating acute infection in HLA-B57/5801-positive subjects drove positive selection of an escape mutation that reverted to wild-type after transmission to HLA-B57/5801-negative individuals. A second escape mutation within the epitope, by contrast, was maintained after transmission. These data show that the process of accumulation of escape mutations within HIV is not inevitable. Complex epitope- and residue-specific selection forces, including CTL-mediated positive selection pressure and virus-mediated purifying selection, operate in tandem to shape HIV evolution at the population level.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1078-8956
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pubmed:author |
pubmed-author:AddoM MMM,
pubmed-author:AllenTT,
pubmed-author:AltfeldMM,
pubmed-author:BrandesBB,
pubmed-author:ChettyPP,
pubmed-author:DixonCC,
pubmed-author:DraenertRR,
pubmed-author:EdwardsAA,
pubmed-author:FeeneyMM,
pubmed-author:GoulderP J RPJ,
pubmed-author:HolmesE CEC,
pubmed-author:JeenaPP,
pubmed-author:KiepielaPP,
pubmed-author:KupferBB,
pubmed-author:LeslieA JAJ,
pubmed-author:LuzziGG,
pubmed-author:LyallHH,
pubmed-author:Martinez-PicadoJJ,
pubmed-author:NovelliVV,
pubmed-author:PfafferottK JKJ,
pubmed-author:PradoJ GJG,
pubmed-author:RamduthDD,
pubmed-author:RoachT ATA,
pubmed-author:St JohnAA,
pubmed-author:TangYY,
pubmed-author:TaylorGG,
pubmed-author:ThomasS ASA,
pubmed-author:Tudor-WilliamsGG,
pubmed-author:WalkerB DBD
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pubmed:issnType |
Print
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
282-9
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:14770175-Adult,
pubmed-meshheading:14770175-Amino Acid Sequence,
pubmed-meshheading:14770175-Child,
pubmed-meshheading:14770175-Epitopes,
pubmed-meshheading:14770175-Evolution, Molecular,
pubmed-meshheading:14770175-Female,
pubmed-meshheading:14770175-Genetic Variation,
pubmed-meshheading:14770175-HIV Infections,
pubmed-meshheading:14770175-HIV-1,
pubmed-meshheading:14770175-HLA-B Antigens,
pubmed-meshheading:14770175-Humans,
pubmed-meshheading:14770175-Infectious Disease Transmission, Vertical,
pubmed-meshheading:14770175-Likelihood Functions,
pubmed-meshheading:14770175-Mutation,
pubmed-meshheading:14770175-Phylogeny,
pubmed-meshheading:14770175-Selection, Genetic,
pubmed-meshheading:14770175-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:14770175-Viral Load
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pubmed:year |
2004
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pubmed:articleTitle |
HIV evolution: CTL escape mutation and reversion after transmission.
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pubmed:affiliation |
Department of Pediatrics, Fuffield Department of Medicine, Peter Medawar Building for Pathogen Research, University of Oxford, Oxford OX1 3SY, UK.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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