HIV-1 Vpr does not inhibit CTL-mediated apoptosis of HIV-1 infected cells

Deborah A. Lewinsohn, Rebecca Lines, David M. Lewinsohn, Stanley R. Riddell, Philip D. Greenberg, Michael Emerman, Steven R. Bartz

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


HIV-1 infected persons develop a robust CTL response to HIV antigens, yet HIV-1 is able to evade this host response and successfully replicate. The mechanism(s) of evasion is not completely defined but has been suggested to include resistance of infected cells to CTL-mediated apoptosis. The HIV-1 Vpr protein induces G2 arrest by indirectly inhibiting activation of cyclin B/p34cdc2 kinase. Granzyme B, the principle mediator of CTL-induced apoptosis, prematurely activates this same kinase complex. Therefore, we assessed the susceptibility of HIV-1 infected cells to CTL-mediated apoptosis to determine whether the expression of Vpr protected the infected cells from CTL-induced apoptosis. Antigen-specific CD8+ CTL were able to induce apoptosis in HIV-1 infected cells and cells labeled with peptide corresponding to the CTL epitope with equivalent efficiency. This demonstrates that neither HIV-1 Vpr nor any other HIV protein directly inhibits CTL effector functions. Furthermore, we confirm that HIV-1 Nef is able to provide partial protection from CTL recognition of infected cells. Thus, the inability of CTL to control HIV-1 infection is likely not due to direct inhibition of CTL-mediated apoptosis.

Original languageEnglish (US)
Pages (from-to)13-21
Number of pages9
Issue number1
StatePublished - 2002


  • Apoptosis
  • CD8 T-lymphocytes
  • Cytotoxic
  • Gene products
  • HIV-1
  • T-lymphocytes
  • Vpr

ASJC Scopus subject areas

  • Virology


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