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Acceleration of virus-induced apoptosis by tumor necrosis factor

A H Koyama1, T Arakawa, A Adachi

  • 1Department of Virology, School of Medicine, The University of Tokushima, Japan. koyama@basic.med.tokushima-u.ac.jp

FEBS Letters
|May 23, 1998
PubMed

Insights

Tumor necrosis factor (TNF) inhibits vesicular stomatitis virus multiplication in HeLa cells. This antiviral effect is linked to TNF accelerating apoptosis, or programmed cell death, in infected cells.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Vesicular stomatitis virus (VSV) is a model virus for studying viral replication.
  • Tumor necrosis factor (TNF) is a cytokine with known antiviral properties.
  • Apoptosis is a form of programmed cell death that can be triggered by various stimuli.

Purpose of the Study:

  • To investigate the effect of TNF on VSV multiplication in HeLa cells.
  • To determine the relationship between TNF-induced apoptosis and VSV replication.
  • To elucidate the mechanism by which TNF inhibits VSV multiplication.

Main Methods:

  • HeLa cells were treated with TNF.
  • Cells were infected with VSV.
  • Virus multiplication and apoptosis kinetics were compared between treated and untreated cells.

Main Results:

  • TNF treatment significantly inhibited VSV multiplication in HeLa cells.
  • TNF treatment led to a rapid induction of apoptosis in VSV-infected cells.
  • The antiviral effect of TNF correlated with the acceleration of apoptosis.

Conclusions:

  • TNF inhibits VSV replication in HeLa cells.
  • The antiviral mechanism of TNF involves the acceleration of apoptosis in infected cells.
  • Targeting apoptotic pathways may represent a strategy for antiviral therapies.

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