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Inhibition of programmed cell death by cytomegaloviruses

Wolfram Brune1

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

Virus Research
|October 26, 2010
PubMed

Insights

Cytomegaloviruses (CMVs) counteract host cell death programs like apoptosis and necrosis. This review details how these viruses, including human CMV (HCMV) and murine CMV (MCMV), use unique genes to suppress programmed cell death (PCD).

Area of Science:

  • Virology
  • Cell Biology
  • Immunology

Background:

  • Programmed cell death (PCD) is an ancient host defense against intracellular pathogens like viruses.
  • Viruses, including large cytomegaloviruses (CMVs), have evolved mechanisms to evade host cell suicide.
  • Human CMV (HCMV) and murine CMV (MCMV) encode proteins that suppress apoptosis and necrosis.

Purpose of the Study:

  • To review the strategies employed by CMVs to inhibit programmed cell death.
  • To identify the signaling pathways targeted by viral anti-PCD mechanisms.
  • To explore the evolutionary origins of viral anti-PCD genes.

Main Methods:

  • Literature review of studies on CMV-mediated cell death suppression.
  • Analysis of identified viral genes encoding apoptosis and necrosis suppressors.
  • Examination of signaling pathways targeted by viral countermeasures.

Main Results:

  • CMVs encode multiple genes that suppress apoptosis and necrosis.
  • Many viral anti-PCD proteins lack homology to cellular counterparts, suggesting independent viral evolution.
  • CMVs target key host cell death signaling pathways.

Conclusions:

  • CMVs possess sophisticated mechanisms to prevent host cell death, ensuring viral replication and persistence.
  • The unique nature of viral anti-PCD genes highlights viral evolutionary adaptations.
  • Understanding these mechanisms provides insights into host-pathogen interactions and potential therapeutic targets.

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