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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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MAVS-MKK7-JNK2 defines a novel apoptotic signaling pathway during viral infection

Yuefeng Huang1, Heng Liu1, Senlin Li1

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

Plos Pathogens
|March 22, 2014
PubMed

Insights

Mitochondrial antiviral signaling protein (MAVS) triggers apoptosis during viral infections by activating the MAVS-MKK7-JNK2 pathway. This pathway is crucial for eliminating infected cells and preventing pathogen spread.

Area of Science:

  • Immunology
  • Cell Biology
  • Virology

Background:

  • Viral infections trigger innate immunity and apoptosis to limit pathogen spread.
  • The precise molecular mechanisms of virus-induced apoptosis remain incompletely understood.
  • Mitochondrial antiviral signaling protein (MAVS) is a key sensor in antiviral innate immunity.

Purpose of the Study:

  • To elucidate the role of MAVS in Sendai virus (SeV)-induced apoptosis.
  • To identify the specific downstream signaling molecules activated by MAVS during viral infection.
  • To investigate the in vivo relevance of the identified pathway in host defense against viral challenge.

Main Methods:

  • Utilized knockout cell lines (Jnk2-/-, Jnk1-/-, Mkk7-/-) to assess apoptosis induction.
  • Investigated protein-protein interactions using co-localization studies on mitochondria.
  • Employed viral challenge models in knockout mice (Jnk2-/-, Jnk1-/-) to evaluate in vivo responses.

Main Results:

  • MAVS is essential for SeV-induced apoptosis, specifically activating c-Jun N-terminal kinase 2 (JNK2).
  • MAVS recruits MAPK kinase 7 (MKK7) to mitochondria, leading to JNK2 phosphorylation and apoptosis.
  • Jnk2-/- mice exhibit severe inflammatory injury post-viral challenge, unlike Jnk1-/- mice.

Conclusions:

  • Identified a novel MAVS-MKK7-JNK2 signaling axis critical for virus-induced apoptosis.
  • Demonstrated the essential role of the mitochondrial outer membrane in orchestrating host antiviral defense.
  • Highlighted JNK2 as a key mediator of apoptosis in response to viral infection.

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