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Related Experiment Videos

HIV expression is induced in dying cells

G E Woloschak1, S Schreck, J Panozzo

  • 1Center for Mechanistic Biology and Biotechnology, Argonne National Laboratory, IL 60439-4833, USA. woloschak@anl.gov

Biochimica Et Biophysica Acta
|March 20, 1997
PubMed
Summary

Cell-killing agents can induce HIV transcription in viable cells, peaking 24 hours after exposure. This HIV-LTR-CAT expression is dose-dependent and linked to cell death, except with gamma rays due to p53 deficiency in HeLa cells.

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Area of Science:

  • Molecular Biology
  • Virology
  • Cell Biology

Background:

  • The human immunodeficiency virus (HIV) long terminal repeat (LTR) is a key regulatory element controlling viral gene expression.
  • Understanding factors that influence HIV transcription is crucial for developing therapeutic strategies.
  • HeLa cells, a common cancer cell line, are often used to study viral replication and gene expression.

Purpose of the Study:

  • To investigate the relationship between cell-killing agents and HIV transcription.
  • To determine if HIV-LTR-CAT construct expression correlates with cell viability and cell death.
  • To explore the role of p53 in gamma-ray-induced HIV transcription in HeLa cells.

Main Methods:

  • HeLa cells stably transfected with an HIV-LTR-CAT construct were exposed to various cell-killing agents.

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  • Chloramphenicol acetyltransferase (CAT) activity was measured as an indicator of HIV-LTR transcription.
  • Cell viability and cell death were assessed following agent exposure.

    • Main Results:

    • A peak in CAT induction was observed in viable cells 24 hours post-exposure to most cell-killing agents.
    • HIV-LTR induction was dose-dependent and correlated with the extent of cell killing.
    • Gamma rays did not induce HIV transcription, likely due to the absence of functional p53 in HeLa cells, which is required for gamma-ray-induced apoptosis.
    • Maximum HIV-LTR-CAT expression occurred at doses causing over 99% cell killing, indicating that cells destined to die were expressing the construct.

    Conclusions:

    • Cell-killing agents, excluding gamma rays in p53-deficient cells, can induce HIV transcription in viable cells.
    • HIV-LTR expression is a marker for cells undergoing lethal damage and eventual cell death.
    • These findings highlight a complex interplay between cellular stress, cell death pathways, and HIV gene regulation.