Human immunodeficiency virus type-1 (HIV-1)- and Epstein-Barr virus specific cytotoxic T lymphocyte precursors exhibit different kinetics in HIV-1-infected persons
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Geretti, AM
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机构:ERASMUS UNIV ROTTERDAM, INST VIROL, 3000 DR ROTTERDAM, NETHERLANDS
Geretti, AM
Dings, MEM
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机构:ERASMUS UNIV ROTTERDAM, INST VIROL, 3000 DR ROTTERDAM, NETHERLANDS
Dings, MEM
vanEls, CACM
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机构:ERASMUS UNIV ROTTERDAM, INST VIROL, 3000 DR ROTTERDAM, NETHERLANDS
vanEls, CACM
vanBaalen, CA
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机构:ERASMUS UNIV ROTTERDAM, INST VIROL, 3000 DR ROTTERDAM, NETHERLANDS
vanBaalen, CA
Wijnholds, FJ
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机构:ERASMUS UNIV ROTTERDAM, INST VIROL, 3000 DR ROTTERDAM, NETHERLANDS
Wijnholds, FJ
Borleffs, JCC
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机构:ERASMUS UNIV ROTTERDAM, INST VIROL, 3000 DR ROTTERDAM, NETHERLANDS
Borleffs, JCC
Osterhaus, ADME
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机构:ERASMUS UNIV ROTTERDAM, INST VIROL, 3000 DR ROTTERDAM, NETHERLANDS
Osterhaus, ADME
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[1] ERASMUS UNIV ROTTERDAM, INST VIROL, 3000 DR ROTTERDAM, NETHERLANDS
[2] NATL INST PUBL HLTH & ENVIRONM PROTECT, LAB VACCINE DEV & IMMUNE MECHANISMS, 3720 BA BILTHOVEN, NETHERLANDS
The frequencies of human immunodeficiency virus type 1 (HIV-1) Gag- and Epstein-Barr virus (EBV)-specific cytotoxic T lymphocyte precursors (CTLp) were studied longitudinally in peripheral blood mononuclear cells from 9 HIV-1-infected persons. By antigen-specific stimulation, HIV-1 Gag-specific CTLp were detected in vitro throughout the course of HIV-1 infection, even after the onset of overt disease. In 4 patients, however, HIV-I Gag-specific CTLp frequencies declined over time in the presence: of maintained EBV-specific CTLp. This decline was correlated with decreasing CD4 (r = .38; P < .05) and CDS (r = .75; P < .001) cell numbers. The maintenance of EBV-specific CTLp in patients with low CD4 cell numbers indicated that EBV-specific CTL-mediated immunity may remain longer unaffected by HIV-1-induced immune dysfunction. Consistent with this observation, the growth of EBV-specific CTL could be supported in vitro by EBV-infected lymphoblastoid B cell lines, independent of both CD4 cells and exogenous cytokines.