The inhibition of pro-apoptotic ICE-like proteases enhances HIV replication

Arul M. Chinnaiyan, Clive Woffendin, Vishva M. Dixit, Gary J. Nabel

Research output: Contribution to journalArticlepeer-review


Accelerated programmed cell death, or apoptosis, contributes to the CD4+ T-cell depletion characteristic of infection by human immunodeficiency virus (HIV). It has therefore been proposed that limiting apoptosis may represent a therapeutic modality for HIV infection. We found, however, that T leukemia cells or peripheral blood mononuclear cells (PBMCs) exposed to HIV-1 underwent enhanced viral replication in the presence of the cell death inhibitor, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD-fmk). Furthermore, z-VAD-fmk, which targets the pro-apoptotic interleukin-1β-converting enzyme (ICE)-like proteases, stimulated endogenous virus production in activated PBMCs derived from HIV-1-infected asymptomatic individuals. These findings suggest that programmed cell death may serve as a beneficial host mechanism to limit HIV spread and that strategies to inhibit it may have deleterious consequences for the infected host.

Original languageEnglish (US)
Pages (from-to)333-337
Number of pages5
JournalNature Medicine
Issue number3
StatePublished - 1997
Externally publishedYes

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)


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