HIV-1-specific CD4+ T cells are detectable in most individuals with active HIV-1 infection, but decline with prolonged vital suppression

Christine J. Pitcher, Claudia Quittner, Dolores M. Peterson, Mark Connors, Richard A. Koup, Vernon C. Maino, Louis J. Picker

Research output: Contribution to journalArticlepeer-review

658 Scopus citations

Abstract

The role of HIV-1-specific CD4+ T-cell responses in controlling HIV-1 infection remains unclear. Previous work has suggested that such cells are eliminated in the early stages of infection in most subjects, and thus cannot substantially contribute to host defense against HIV-1. Here, using flow cytometric detection of antigen-induced intracellular cytokines, we show that significant frequencies of gag specific, T-helper-1 CD4+ memory T cells are detectable in most subjects with active/progressive HIV-1 infection (median frequency, 0.12% of memory subset; range, 0-0.66%). Median frequencies of these cells were considerably higher in nonprogressive HIV-1 disease (0.40%), but there was substantial overlap between the two groups (range of nonprogressors, 0.10-1.7%). Continuous HIV-1 suppression with anti- retroviral therapy was associated with a time-dependent reduction in median frequencies of gag-specific CD4+ memory T cells: 0.08% in subjects treated for 4-24 weeks, and 0.03% in subjects treated for 47-112 weeks. Thus, functional HIV-1-specific CD4+ T cells are commonly available for support of anti-HIV-1 effector responses in active disease, but their decline with anti- retroviral therapy indicates that immunologic participation in long-term HIV- 1 control will probably require effective vaccination strategies.

Original languageEnglish (US)
Pages (from-to)518-525
Number of pages8
JournalNature medicine
Volume5
Issue number5
DOIs
StatePublished - May 1999

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Fingerprint Dive into the research topics of 'HIV-1-specific CD4<sup>+</sup> T cells are detectable in most individuals with active HIV-1 infection, but decline with prolonged vital suppression'. Together they form a unique fingerprint.

Cite this