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Research Article Free access | 10.1172/JCI117105

Programmed death of T cells in human immunodeficiency virus infection. No correlation with progression to disease.

L Meyaard, S A Otto, I P Keet, M T Roos, and F Miedema

Department of Clinical Viro-Immunology, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam.

Find articles by Meyaard, L. in: PubMed | Google Scholar

Department of Clinical Viro-Immunology, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam.

Find articles by Otto, S. in: PubMed | Google Scholar

Department of Clinical Viro-Immunology, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam.

Find articles by Keet, I. in: PubMed | Google Scholar

Department of Clinical Viro-Immunology, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam.

Find articles by Roos, M. in: PubMed | Google Scholar

Department of Clinical Viro-Immunology, Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam.

Find articles by Miedema, F. in: PubMed | Google Scholar

Published March 1, 1994 - More info

Published in Volume 93, Issue 3 on March 1, 1994
J Clin Invest. 1994;93(3):982–988. https://doi.org/10.1172/JCI117105.
© 1994 The American Society for Clinical Investigation
Published March 1, 1994 - Version history
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Abstract

Programmed death of T cells has been proposed as one of the mechanisms by which HIV affects immune functions in stages of infection where the number of infected cells is low. Indeed, in HIV-infected individuals both CD4+ and CD8+ T cells are primed for programmed cell death, which can be enhanced by polyclonal stimulation. Here, we investigated programmed death of T cells in all stages of HIV infection, including acute infection. In individuals with primary infection the number of T cells dying due to apoptosis was much higher than in the asymptomatic phase of infection and paralleled increased numbers of CD8+ cells. In asymptomatic HIV-infected individuals, cells were dying in increased percentages compared with noninfected controls, although at much lower numbers than during acute infection. Death of T cells was not quantitatively correlated with CD4+ T cell numbers or appearance of more cytopathic, syncytium-inducing HIV variants. Analysis of the phenotype of cells undergoing apoptosis revealed that cell death was not confined to a specific T cell subset nor correlated with expression of certain T cell activation markers. Our results imply that the extent of programmed cell death of T cells in HIV infection does not correlate with progression to disease.

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