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An autoinhibitory mechanism modulates MAVS activity in antiviral innate immune response

Yuheng Shi1, Bofeng Yuan1, Nan Qi1

  • 1State Key Laboratory of Cell Biology, Innovation Center for Cell Signaling Network, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.

Nature Communications
|July 18, 2015
PubMed

Insights

RIG-I activates MAVS to restrict viral infections. MAVS forms filaments, releasing autoinhibitory regions to activate antiviral signaling pathways like IRF3 and NF-κB.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • RIG-I (Retinoic acid-inducible gene I) recognizes viral RNA during infection.
  • Activated RIG-I triggers the adaptor protein MAVS (Mitochondrial antiviral signaling protein).
  • MAVS forms prion-like filaments to initiate antiviral signaling, leading to type I interferon production.

Purpose of the Study:

  • To elucidate the regulatory mechanisms governing MAVS activity.
  • To identify specific MAVS regions responsible for activating key transcription factors.
  • To understand how MAVS activity is controlled in both quiescent and stimulated states.

Main Methods:

  • Functional mapping of MAVS to identify distinct activation domains.
  • Analysis of MAVS interactions with TNF receptor-associated factors (TRAFs).
  • Investigation of intramolecular regulation within the MAVS protein.

Main Results:

  • Distinct regions within MAVS were identified for activating IRF3 (interferon regulatory factor 3) and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells).
  • These regions preferentially recruit specific TRAFs to mediate downstream signaling.
  • Adjacent regions were found to autoinhibit the activity of these MAVS domains in unstimulated cells.

Conclusions:

  • MAVS activity is regulated by an autoinhibitory mechanism in quiescent cells.
  • Viral infection and MAVS filament formation release these inhibitory constraints.
  • This regulated activation allows for precise control of antiviral signaling cascades, including type I interferon production.

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