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Updated: Aug 25, 2025

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
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Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production

Published on: March 2, 2014

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Shielding the mRNA-translation factor eIF2B from inhibitory p-eIF2 as a viral strategy to evade protein kinase

Jennifer D Wuerth1, Friedemann Weber2

  • 1Institute of Innate Immunity, Medical Faculty, University of Bonn, 53127 Bonn, Germany.

Current Opinion in Immunology
|October 15, 2022
PubMed

Insights

Viruses have evolved a new strategy to evade the immune system. Certain viral proteins activate PKR and eIF2 phosphorylation but protect eIF2B, allowing translation during an activated integrated stress response.

Area of Science:

  • Virology
  • Immunology
  • Molecular Biology

Background:

  • The interferon-regulated kinase PKR is a key innate immune factor against viral infections.
  • PKR initiates the integrated stress response (ISR) by phosphorylating eIF2, inhibiting translation.
  • Viruses typically evade PKR by interfering with its activation or eIF2 phosphorylation.

Purpose of the Study:

  • To describe a novel viral evasion strategy that circumvents PKR-mediated translational shutdown.
  • To investigate how certain RNA viruses maintain mRNA translation despite PKR activation.

Main Methods:

  • The study likely involved molecular biology techniques to analyze protein interactions and cellular responses.
  • Investigated the interplay between viral proteins, PKR, eIF2, and eIF2B.

Main Results:

  • Proteins from three distinct RNA viruses were found to allow PKR activation and eIF2 phosphorylation.
  • These viral proteins protect eIF2B from inhibition by phosphorylated eIF2.
  • This mechanism enables viral mRNA translation even during an activated ISR.

Conclusions:

  • A novel viral immune evasion strategy involves protecting eIF2B from PKR-induced inhibition.
  • This allows viruses to overcome the host's integrated stress response and continue replication.
  • This finding expands our understanding of virus-host interactions and innate immunity.

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