HIV infection induces changes in CD4+ T-cell phenotype and depletions within the CD4+ T-cell repertoire that are not immediately restored ... View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-05

AUTHORS

Mark Connors, Joseph A. Kovacs, Seth Krevat, Juan C. Gea-Banacloche, Michael C. Sneller, Mark Flanigan, Julia A. Metcalf, Robert E. Walker, Judith Falloon, Michael Baseler, Randy Stevens, Irwin Feuerstein, Henry Masur, H. Clifford Lane

ABSTRACT

Changes in CD4+ T-cell surface marker phenotype and antigen receptor (TCR) repertoire were examined during the course of HIV infection and following therapy. A preferential decline in naive CD4+ T cells was noted as disease progressed. Following protease inhibitor therapy, naive CD4+ T cells increased only if they were present before initiation of therapy. Disruptions of the CD4+ TCR repertoire were most prevalent in patients with the lowest CD4+ T-cell counts. Antiviral or IL-12 therapy-induced increases in CD4+ T-cell counts led to only minor changes in previously disrupted repertoires. Thus, CD4+ T-cell death mediated by HIV-1 infection may result in a preferential decline in the number of naive CD4+ T cells and disruptions of the CD4+T-cell repertoire that are not immediately corrected by antiviral or immune-based therapies. More... »

PAGES

533-540

Journal

TITLE

Nature Medicine

ISSUE

5

VOLUME

3

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm0597-533

    DOI

    http://dx.doi.org/10.1038/nm0597-533

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/9142122


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    21 schema:description Changes in CD4+ T-cell surface marker phenotype and antigen receptor (TCR) repertoire were examined during the course of HIV infection and following therapy. A preferential decline in naive CD4+ T cells was noted as disease progressed. Following protease inhibitor therapy, naive CD4+ T cells increased only if they were present before initiation of therapy. Disruptions of the CD4+ TCR repertoire were most prevalent in patients with the lowest CD4+ T-cell counts. Antiviral or IL-12 therapy-induced increases in CD4+ T-cell counts led to only minor changes in previously disrupted repertoires. Thus, CD4+ T-cell death mediated by HIV-1 infection may result in a preferential decline in the number of naive CD4+ T cells and disruptions of the CD4+T-cell repertoire that are not immediately corrected by antiviral or immune-based therapies.
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