Characterization of virus-specific CD8(+) effector T cells in the course of HIV-1 infection : longitudinal analyses in slow and rapid progressors
Studies in humans have provided evidence that CD8(+) T cells exhibit distinct phenotypical and functional properties dependent on virus specificity. It is not known how these T-cell phenotypes develop over the course of infection. Dynamics and properties of T cells specific for human immunodeficienc...
| Publié dans: | Clinical immunology (Orlando, Fla.). - 1999. - 113(2004), 3 vom: 12. Dez., Seite 299-309 |
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| Auteur principal: | |
| Autres auteurs: | , , , , , |
| Format: | Article |
| Langue: | English |
| Publié: |
2004
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| Accès à la collection: | Clinical immunology (Orlando, Fla.) |
| Sujets: | Journal Article Research Support, Non-U.S. Gov't Membrane Glycoproteins Pore Forming Cytotoxic Proteins Tumor Necrosis Factor Receptor Superfamily, Member 7 Perforin 126465-35-8 GZMB protein, human EC 3.4.21.- Granzymes |
| Résumé: | Studies in humans have provided evidence that CD8(+) T cells exhibit distinct phenotypical and functional properties dependent on virus specificity. It is not known how these T-cell phenotypes develop over the course of infection. Dynamics and properties of T cells specific for human immunodeficiency virus (HIV), cytomegalovirus (CMV), and Epstein-Barr virus (EBV) in HIV infection were investigated in relation to viral load. In rapid progressors, HIV-specific CD8(+) T cells were less differentiated early in infection and did not develop a more differentiated phenotype. In slow progressors, perforin expression of HIV-specific CD8(+) T cells slightly increased over time. HIV and EBV loads were detectable in all individuals, while CMV load could not be detected. Thus, in individuals with progressive HIV infection, HIV-specific T cells are less differentiated already early in infection. This apparent block in differentiation may be partly caused by chronic viremia or lack of CD4(+) T-cell help |
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| Description: | Date Completed 15.12.2004 Date Revised 16.11.2017 published: Print Citation Status MEDLINE |
| ISSN: | 1521-7035 |