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Varicella-zoster virus induces apoptosis in cell culture

C Sadzot-Delvaux1, P Thonard, S Schoonbroodt

  • 1Department of Microbiology, University of Liège, Belgium.

The Journal of General Virology
|November 1, 1995
PubMed

Insights

Varicella-zoster virus (VZV) infection triggers apoptosis, a programmed cell death. This VZV-induced apoptosis, marked by DNA fragmentation, appears independent of Bcl-2, a known apoptosis inhibitor.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Apoptosis, or programmed cell death, is a critical cellular process activated by various stimuli, including viral infections.
  • Varicella-zoster virus (VZV), a human herpesvirus, is known to establish lifelong latency in sensory ganglia.
  • Understanding virus-induced apoptosis is crucial for comprehending viral pathogenesis and latency.

Purpose of the Study:

  • To investigate the mechanism of cell death induced by lytic varicella-zoster virus (VZV) infection.
  • To determine if VZV-induced cell death is mediated by apoptosis.
  • To explore potential cellular or viral factors involved in VZV latency, particularly in relation to apoptosis evasion.

Main Methods:

  • Induction of lytic VZV infection in vitro.
  • Analysis of cellular DNA fragmentation (oligonucleosomal fragments).
  • Assessment of chromatin condensation.
  • Evaluation of VZV-induced cell death in relation to apoptosis pathways, including Bcl-2.

Main Results:

  • Lytic VZV infection in vitro is characterized by nuclear DNA fragmentation into oligonucleosomal fragments.
  • Chromatin condensation is observed during VZV infection.
  • VZV-induced cell death in vitro is mediated by apoptosis.
  • The VZV apoptosis mechanism appears independent of Bcl-2, a common inhibitor of apoptosis.

Conclusions:

  • Varicella-zoster virus actively induces apoptosis in infected cells.
  • The apoptotic pathway activated by VZV involves DNA fragmentation and chromatin condensation.
  • The observed apoptosis mechanism in VZV infection does not seem to involve Bcl-2, suggesting alternative evasion strategies for VZV latency.

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