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Prevention of cellular suicide by cytomegaloviruses

Patricia M Fliss1, Wolfram Brune

  • 1Heinrich Pette Institute, Leibniz Institute for Experimental Virology, Martinistr. 52, 20251 Hamburg, Germany. patricia.fliss@hpi.uni-hamburg.de

Viruses
|December 4, 2012
PubMed

Insights

Cytomegaloviruses (CMVs) encode viral cell death inhibitors to maintain host cell viability for replication. This review details how CMVs, including murine CMV (MCMV), use inhibitors like vICA, vMIA, vIBO, and vIRS to block apoptosis and programmed necrosis.

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Viruses depend on host cells for replication, making programmed cell death (PCD) a key antiviral defense.
  • Slowly replicating viruses like cytomegaloviruses (CMVs) require sustained host cell viability.
  • CMVs have evolved mechanisms to counteract host-induced PCD.

Purpose of the Study:

  • To review known cell death suppressors encoded by CMVs.
  • To elucidate the mechanisms of action of these viral inhibitors.
  • To highlight the importance of inhibiting apoptosis and programmed necrosis during CMV infection.

Main Methods:

  • Literature review of scientific publications on CMV and cell death.
  • Analysis of viral genomes for cell death inhibitor genes.
  • Examination of experimental data on the function of viral inhibitors.

Main Results:

  • CMVs encode multiple inhibitors targeting apoptosis (vICA, vMIA, vIBO) and programmed necrosis (vIRS).
  • These inhibitors interfere with key regulators of both extrinsic and intrinsic apoptosis pathways.
  • Murine CMV (MCMV) encodes vIRS, indicating the significance of blocking programmed necrosis.

Conclusions:

  • CMV-encoded inhibitors are crucial for viral replication by preserving host cell viability.
  • Understanding these viral countermeasures provides insights into host-pathogen interactions.
  • Targeting these inhibitors could represent a novel antiviral therapeutic strategy.

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