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A prion-like trigger of antiviral signaling

Junqiang Ye1, Tom Maniatis

  • 1Department of Molecular and Cellular Biology, Harvard University, Cambridge, MA 02138, USA.

Cell
|August 6, 2011
PubMed

Insights

Virus infection causes the MAVS protein to change shape, forming prion-like aggregates. These self-aggregates act as sensitive triggers for antiviral signaling pathways.

Area of Science:

  • Immunology
  • Molecular Biology
  • Virology

Background:

  • Mitochondrial antiviral signaling (MAVS) protein is crucial for innate antiviral immunity.
  • MAVS initiates signaling cascades upon viral detection.
  • The precise mechanism of MAVS activation remained unclear.

Discussion:

  • Virus infection induces a conformational change in MAVS.
  • This change promotes prion-like self-aggregation of MAVS.
  • These aggregates form functional signaling complexes on mitochondria.

Key Insights:

  • MAVS activation is a prion-like process.
  • Self-aggregation of MAVS is essential for its function.
  • This mechanism provides a sensitive trigger for antiviral responses.

Outlook:

  • Understanding MAVS aggregation may reveal new therapeutic targets.
  • Further research into prion-like mechanisms in immunity is warranted.
  • This finding deepens our comprehension of host-pathogen interactions.

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