Human immunodeficiency virus type 1 induces apoptosis in CD4+ but not in CD8+ T cells in ex vivo-infected human lymphoid tissue

J. C. Grivel, N. Malkevitch, L. Margolis

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

Progression of human immunodeficiency virus (HIV) disease is associated with massive death of CD4+ T cells along with death and/or dysfunction of CD8+ T cells. In vivo, both HIV infection per se and host factors may contribute to the death and/or dysfunction of CD4+ and CD8+ T cells. Progression of HIV disease is often characterized by a switch from R5 to X4 HIV type 1 (HIV-1) variants. In human lymphoid tissues ex vivo, it was shown that HIV infection is sufficient for CD4+ T-cell depletion. Here we address the question of whether infection of human lymphoid tissue ex vivo with prototypic R5 or X4 HIV variants also depletes or impairs CD8+ T cells. We report that whereas productive infection of lymphoid tissue ex vivo with R5 and X4 HIV-1 isolates induced apoptosis in CD4+ T cells, neither viral isolate induced apoptosis in CD8+ T cells. Moreover, in both infected and control tissues we found similar numbers of CD8+ T cells and similar production of cytokines by these cells in response to phorbol myristate acetate or anti-CD3-anti-CD28 stimulation. Thus, whereas HIV-1 infection per se in human lymphoid tissue is sufficient to trigger apoptosis in CD4+ T-cells, the death of CD8+ T cells apparently requires additional factors.

Original languageEnglish
Pages (from-to)8077-8084
Number of pages8
JournalJournal of Virology
Volume74
Issue number17
DOIs
Publication statusPublished - 2000
Externally publishedYes

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Lymphoid Tissue
HIV-1
Apoptosis
T-Lymphocytes
Virus Diseases
HIV
Tetradecanoylphorbol Acetate
Infection
Cell Death
Cytokines

ASJC Scopus subject areas

  • Immunology

Cite this

Human immunodeficiency virus type 1 induces apoptosis in CD4+ but not in CD8+ T cells in ex vivo-infected human lymphoid tissue. / Grivel, J. C.; Malkevitch, N.; Margolis, L.

In: Journal of Virology, Vol. 74, No. 17, 2000, p. 8077-8084.

Research output: Contribution to journalArticle

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