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

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

The specific and essential role of MAVS in antiviral innate immune responses

Qinmiao Sun1, Lijun Sun, Hong-Hsing Liu

  • 1Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

Immunity
|May 23, 2006
PubMed

Insights

Mitochondrial antiviral signaling protein (MAVS) is crucial for innate immunity against viruses. MAVS deficiency in mice blocks interferon production and antiviral responses, confirming its essential role in vivo.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Mitochondrial antiviral signaling protein (MAVS) is known to mediate antiviral responses.
  • In vitro studies suggest MAVS involvement in interferon induction by cytosolic DNA, but in vivo data are limited.

Purpose of the Study:

  • To investigate the in vivo role of MAVS in innate immune responses to viral infections.
  • To determine if MAVS is essential for interferon induction by cytosolic DNA.

Main Methods:

  • Generation and analysis of MAVS-deficient mice.
  • Assessment of NF-kappaB and IRF activation.
  • Evaluation of interferon induction upon viral and cytosolic DNA stimulation.
  • Testing immune defense against viral challenge.

Main Results:

  • MAVS deficiency abolished viral induction of interferons and NF-kappaB/IRF3 activation in most cell types, excluding pDCs.
  • MAVS was not required for interferon induction by cytosolic DNA or Listeria monocytogenes.
  • MAVS-deficient mice showed impaired interferon response to poly(I:C) and compromised antiviral immunity.

Conclusions:

  • MAVS is essential in vivo for the cytosolic viral signaling pathway mediating innate immune responses to viral infections.
  • The role of MAVS in interferon induction by cytosolic DNA is not supported by in vivo evidence.

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