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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0007584,
umls-concept:C0019682,
umls-concept:C0019699,
umls-concept:C0021311,
umls-concept:C0025260,
umls-concept:C0039194,
umls-concept:C0039195,
umls-concept:C0332281,
umls-concept:C0332307,
umls-concept:C0392747,
umls-concept:C0443172,
umls-concept:C0449258,
umls-concept:C0871261,
umls-concept:C1332714,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
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pubmed:issue |
16
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pubmed:dateCreated |
1999-1-28
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pubmed:abstractText |
We investigated memory cytotoxic T lymphocyte (CTLm) responses to HIV-1 as a determinant of HIV-1 disease progression, in relation to plasma HIV-1 load and T lymphocyte numbers in a longitudinal study of 14 homosexual men with incident HIV-1 infection. Study participants were selected who exhibited failure of T cell homeostasis, i.e., a downward inflection in CD3+ T cells that occurs in >75% of persons 1.5 to 2.5 years before development of AIDS, and compared with participants who developed low CD4+ T cell counts associated with possible T cell homeostasis failure, a subject who progressed rapidly to AIDS without well-defined T cell inflection, and subjects who had long-term preservation of T cell homeostasis (nonprogressors). High CTLm responses against Gag, but not Pol or Env, soon after seroconversion were associated with a slower loss of CD4+ T cells 1-4 years after seroconversion. Anti-Env CTLm responses decreased in most subjects around the time that T cell homeostasis failed. Plasma HIV-1 RNA increased exponentially (1.59-fold per year) over the 5 years preceding failure of T cell homeostasis, and there was a shift from a non-syncytium-inducing/CCR5 coreceptor phenotype of HIV-1 to a syncytium-inducing/CXCR4 phenotype, regardless of high or increasing levels of anti-HIV-1 CTLm during this time. These observations suggest that decreases in CTLm and increasing virus load are independent factors contributing to HIV-1 disease progression.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0889-2229
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
14
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1423-33
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:9824320-CD4 Lymphocyte Count,
pubmed-meshheading:9824320-CD4-Positive T-Lymphocytes,
pubmed-meshheading:9824320-Disease Progression,
pubmed-meshheading:9824320-HIV Infections,
pubmed-meshheading:9824320-HIV-1,
pubmed-meshheading:9824320-Homeostasis,
pubmed-meshheading:9824320-Humans,
pubmed-meshheading:9824320-Immunologic Memory,
pubmed-meshheading:9824320-Longitudinal Studies,
pubmed-meshheading:9824320-Male,
pubmed-meshheading:9824320-Phenotype,
pubmed-meshheading:9824320-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:9824320-Viral Load,
pubmed-meshheading:9824320-Viremia
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pubmed:year |
1998
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pubmed:articleTitle |
Anti-HIV type 1 memory cytotoxic T lymphocyte responses associated with changes in CD4+ T cell numbers in progression of HIV type 1 infection.
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pubmed:affiliation |
University of Pittsburgh School of Medicine, Pennsylvania 15261, USA.
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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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