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Viral subversion of apoptotic enzymes: escape from death row

Sonja M Best1

  • 1Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA. sbest@niaid.nih.gov

Annual Review of Microbiology
|August 30, 2008
PubMed

Insights

Viruses inhibit host cell death pathways, like apoptosis, to replicate. However, some viruses use these same pathways for their own life cycle, revealing a complex relationship.

Area of Science:

  • Virology
  • Molecular Biology
  • Cellular Biology

Background:

  • Viruses manipulate host cell machinery for survival and replication.
  • Apoptosis, or programmed cell death, is a crucial host defense mechanism.
  • Cellular proteases, including caspases and serine proteases, are key regulators of apoptosis.

Purpose of the Study:

  • To explore viral strategies for inhibiting host apoptosis.
  • To investigate the diverse roles of caspases in viral replication.
  • To understand the complex interplay between viruses and apoptosis.

Main Methods:

  • Review of viral inhibitor classes targeting caspases (serpins, p35, IAPs, vFLIPs).
  • Analysis of viral subversion of serine proteases (granzyme B, HtrA2/Omi).
  • Examination of viruses utilizing caspases for replication processes.

Main Results:

  • Viruses employ multiple mechanisms to suppress apoptosis, targeting caspases and serine proteases.
  • Viral inhibitors like serpins, p35, IAPs, and vFLIPs antagonize caspase activity.
  • Some viruses paradoxically utilize caspases for viral protein maturation and progeny release.

Conclusions:

  • Viruses exhibit a multifaceted relationship with host apoptosis, both inhibiting and utilizing it.
  • Understanding these interactions is vital for comprehending virus pathogenesis.
  • Studying viral modulation of apoptosis provides insights into cellular death regulation.

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