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Control of apoptosis by human cytomegalovirus

A L McCormick1

  • 1Department of Microbiology & Immunology, Emory Vaccine Center, Emory University Atlanta, GA 30322, USA. louise.mccormick@emory.edu

Current Topics in Microbiology and Immunology
|July 22, 2008
PubMed

Insights

Cytomegaloviruses (CMVs) encode multiple proteins that inhibit programmed cell death (apoptosis) to ensure viral survival. These viral factors collectively counteract host defenses, allowing the virus to replicate effectively.

Area of Science:

  • Virology
  • Immunology
  • Cell Biology

Background:

  • Caspase-dependent apoptosis is a crucial host defense against viral infections.
  • Viruses frequently encode proteins to subvert apoptosis and promote their replication.
  • Cytomegaloviruses (CMVs) are known to manipulate host cell death pathways.

Purpose of the Study:

  • To investigate the mechanisms by which Cytomegaloviruses (CMVs) evade caspase-dependent apoptosis.
  • To identify specific viral gene products involved in inhibiting host cell death.
  • To understand how CMV manipulates intrinsic and extrinsic apoptosis pathways.

Main Methods:

  • Analysis of viral mutants lacking specific apoptosis-inhibiting genes (vMIA, vICA, pUL38, IE1, IE2, UL38, M45, m41).
  • Assessment of viral RNA (beta2.7) function in maintaining cellular ATP production.
  • Evaluation of viral protein roles in preventing apoptosis induced by various stimuli.

Main Results:

  • CMV encodes vMIA and vICA, which are essential and sufficient to inhibit apoptosis.
  • Other viral proteins like pUL38, IE1, and IE2 also contribute to preventing apoptosis.
  • Deletion mutants of UL38, M45, or m41 exhibit increased susceptibility to apoptosis.
  • Viral RNA beta2.7 maintains ATP production and prevents mitochondrial poison-induced death.

Conclusions:

  • CMV employs a multi-pronged strategy involving multiple viral gene products to inhibit apoptosis.
  • These viral factors collectively control death-inducing stimuli, ensuring infected cell survival and viral propagation.
  • CMV effectively alters host cell intrinsic defenses to promote viral replication.

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