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Caspase-3-like proteases are activated by infection but are not required for replication of vesicular stomatitis

J A Hobbs1, R H Schloemer, G Hommel-Berrey

  • 1Department of Microbiology and Immunology, Indiana University School of Medicine, 702 Barnhill Dr., Riley Hospital Rm. 0615, Indianapolis, IN 46202-5200, USA.

Virus Research
|October 13, 2001
PubMed

Insights

Vesicular stomatitis virus (VSV) infection triggers apoptosis, a programmed cell death. However, inhibiting apoptosis did not affect VSV replication, suggesting it may aid viral spread.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Vesicular stomatitis virus (VSV), a rhabdovirus, induces DNA fragmentation, a hallmark of apoptosis.
  • The precise role of apoptosis in the VSV-host interaction and viral replication remains largely undefined.

Purpose of the Study:

  • To investigate the role of apoptosis in VSV infection and its impact on viral replication.
  • To determine if inhibiting apoptosis affects VSV titers and progeny production.

Main Methods:

  • Infection of Jurkat T cells with VSV.
  • Assessing apoptotic events including caspase activation, PARP cleavage, and DNA fragmentation.
  • Utilizing apoptosis inhibitors to evaluate their effect on viral replication.

Main Results:

  • VSV infection activated caspases-3 and -7, leading to PARP cleavage, DNA fragmentation, and membrane damage.
  • Apoptosis inhibition blocked DNA fragmentation and PARP cleavage but did not reduce viral titers.
  • Caspase activation is essential for VSV-induced apoptosis but not for in vitro viral replication.

Conclusions:

  • Apoptosis is not essential for VSV replication in vitro.
  • VSV-induced apoptosis may represent a host defense mechanism or a viral strategy for in vivo dissemination.

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