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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

STAT protein interference and suppression of cytokine signal transduction by measles virus V protein

Heidi Palosaari1, Jean-Patrick Parisien, Jason J Rodriguez

  • 1Immunobiology Center, Mount Sinai School of Medicine, One Gustave L. Levy Pl., Box 1630, New York, NY 10029, USA.

Journal of Virology
|June 14, 2003
PubMed

Insights

Measles virus V protein blocks host STAT signaling, inhibiting interferon responses. This mechanism contributes to measles-induced immune suppression and susceptibility to infections.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • Measles virus causes significant global mortality and morbidity annually.
  • Measles infection leads to immune suppression, increasing susceptibility to opportunistic infections.
  • Cytokine signaling pathways are crucial for effective immune responses.

Purpose of the Study:

  • To investigate the mechanism by which measles virus inhibits host cytokine responses.
  • To determine the role of measles virus V protein in interfering with host signaling pathways.
  • To elucidate how measles virus evades immune detection and suppression.

Main Methods:

  • Studied the effect of measles virus V protein expression on interferon-induced transcriptional responses.
  • Investigated interference with signaling pathways of interleukin-6 and v-Src.
  • Used affinity purification to identify measles V protein interacting partners, including STAT proteins.
  • Performed mechanistic studies to assess STAT protein phosphorylation and nuclear accumulation.

Main Results:

  • Measles virus V protein expression inhibits alpha, beta, and gamma interferon-induced transcriptional responses.
  • The V protein interferes with signaling by interleukin-6 and v-Src.
  • Measles V protein associates with cellular STAT1, STAT2, STAT3, and IRF9.
  • The V protein causes a defect in interferon-induced STAT nuclear accumulation, with STAT proteins found in cytoplasmic bodies in infected cells.

Conclusions:

  • Measles virus directly interferes with host STAT protein-dependent signaling systems to inhibit cytokine responses.
  • The V protein's interference with STAT nuclear accumulation is a key mechanism for immune evasion.
  • This interference with STAT-inducible transcription links innate immune evasion to adaptive immune suppression in measles virus infection.

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