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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
08:32

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The mitochondrial antiviral signaling protein, MAVS, is cleaved during apoptosis

Iain Scott1, Kristi L Norris

  • 1Biochemistry Section, Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Room 2C-1014, Building 35, 9000 Rockville Pike, Bethesda, MD 20892, USA. scotti@ninds.nih.gov

Biochemical and Biophysical Research Communications
|August 12, 2008
PubMed

Insights

Host cell apoptosis limits viral infection. We found that MAVS protein cleavage occurs during apoptosis, suggesting a role in viral defense.

Area of Science:

  • Innate immunity
  • Apoptosis regulation
  • Mitochondrial signaling

Background:

  • Virus-infected cells undergo apoptosis as a host defense mechanism.
  • MAVS (Mitochondrial antiviral signaling protein) is a key innate immune signaling molecule localized to mitochondria.
  • Mitochondria play a crucial role in regulating apoptosis.

Purpose of the Study:

  • To investigate the role of MAVS in the process of apoptosis.
  • To determine if MAVS undergoes changes during apoptosis and if this is relevant to viral infection.

Main Methods:

  • Induction of cell death and monitoring MAVS protein.
  • Use of proteasome and caspase inhibitors.
  • Transfection with viral dsRNA and dsDNA.
  • Over-expression of anti-apoptotic Bcl-xL.

Main Results:

  • MAVS protein is rapidly cleaved during apoptosis, leading to its release from the outer mitochondrial membrane.
  • This MAVS cleavage is inhibited by proteasome and caspase inhibitors.
  • Viral dsRNA and dsDNA induce MAVS cleavage, suggesting its importance during viral infections.
  • Blocking apoptosis with Bcl-xL prevents MAVS cleavage, indicating it occurs downstream of caspase activation.

Conclusions:

  • MAVS undergoes caspase-dependent cleavage during apoptosis.
  • MAVS cleavage is a potential host response to viral infection.
  • This cleavage is an integral part of the apoptotic program, occurring downstream of caspase activation.

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