Mapping of HIV-1 determinants of apoptosis in infected T cells

Eric Rapaport, Carolyn R. Casella, David Iklé, Farah Mustafa, Dale Isaak, Terri H. Finkel

Research output: Contribution to journalArticlepeer-review

17 Citations (Scopus)


HIV-1 infection leads to death of CD4+ T cells in vivo and in vitro, although the mechanisms of this cell death are not well defined. We used flow cytometry to concurrently analyze infection and apoptosis of the CD4+ CEM T cell line and human peripheral blood mononuclear cells (PBMC). Surprisingly, T cells productively infected with HIV-1 IIIB showed less apoptosis than control, uninfected T cells. This relative paucity of apoptosis was a characteristic of IIIB, since a large number of cells infected with the viral clone, HIV-1 NL4-3, were apoptotic. The nef, vpr, and vpu gene products were not responsible for apoptosis of NL4-3-infected cells, since NL4- 3ΔVprΔVpuΔNef and HXB-2 (a nef, vpr, and vpu triple mutant derived from IIIB) also killed infected cells. Moreover, only IIIB-infected cells showed a resistance to background levels of apoptosis. Thus, the apoptotic (and antiapoptotic) properties of HIV-1 do not map solely to mutations in nef, vpr, or vpu. We postulate that, in vivo, HIV variants that do not induce rapid apoptosis in the cells they infect may have a selective advantage.

Original languageEnglish
Pages (from-to)407-417
Number of pages11
Issue number2
Publication statusPublished - Dec 20 1998
Externally publishedYes


  • Apoptosis
  • Flow cytometry
  • Gene products: vpr, vpu, nef
  • HIV-1
  • T lymphocytes

ASJC Scopus subject areas

  • Virology


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