NLM Gateway
A service of the U.S. National Institutes of Health
Your Entrance to
Resources from the
National Library of Medicine
    Home      Term Finder      Limits/Settings      Search Details      History      My Locker        About      Help      FAQ    
Skip Navigation Side Barintended for web crawlers only

Modulation of bcl-2 expression in HIV-infected U937 cells.

Mathew P, Badley A, McElhinny J, Leibson P, Paya CV; National Conference on Human Retroviruses and Related Infections.

Program Abstr Second Natl Conf Hum Retrovir Relat Infect Natl Conf Hum Retrovir Relat Infect 2nd 1995 Wash DC. 1995 Jan 29-Feb 2; 135.

Mayo Clinic, Rochester, MN.

The major reservoir for persistent viral replication in human immunodeficiency virus (HIV)-infected individuals is the monocyte-macrophage system. The promonocytic U937 cell line provides a model for the understanding of viral persistence. U937 cells infected with HIV undergo apoptotic cell death, but surviving populations show continued viral replication. While bcl-2 is known to inhibit apoptosis and function as an anti-oxidant molecule, intracellular oxidative mechanisms activate HIV replication. In Epstein- Barr virus (EBV)-infected B cells, HIV has been indirectly associated with decreased bcl-2 expression via the downregulation of EBV proteins. In this study, we analyzed the expression of bcl-2 in HIV-infected monocytic cells in relationship to HIV-induced cell death and viral persistence. Within 5 days post-infection, bcl-2 protein levels decrease, and this correlates with cell death. By different methods we determined that HIV-mediated U937 death is due to apoptosis. Surviving U937 cells exhibit persistent viral replication as assayed by reverse transcriptase and p24 ELISA, and in this population, decreased bcl-2 expression is maintained. Our studies demonstrate that 1) HIV can, in the absence of interaction with other viruses, modulate bcl-2 expression; and 2) decreased bcl-2 expression is associated with apoptotic cell death and subsequent viral persistence in U937 cells. Whether manipulation of bcl-2 expression in U937 cells can modulate apoptosis or viral persistence is currently being explored.

Publication Types:
  • Meeting Abstracts
Keywords:
  • AIDS Vaccines
  • Acquired Immunodeficiency Syndrome
  • Apoptosis
  • Cell Line
  • Down-Regulation
  • Gene Expression
  • HIV
  • HIV Core Protein p24
  • HIV Infections
  • HIV Long Terminal Repeat
  • HIV Protease
  • HIV Seropositivity
  • Humans
  • Monocytes
  • U937 Cells
  • genetics
  • immunology
Other ID:
  • 95920468
UI: 102213417

From Meeting Abstracts




Contact Us
U.S. National Library of Medicine |  National Institutes of Health |  Health & Human Services
Privacy |  Copyright |  Accessibility |  Freedom of Information Act |  USA.gov