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Trends Immunol. 2014 Sep;35(9):420-8. doi: 10.1016/j.it.2014.07.006. Epub 2014 Aug 19.

Antiviral innate immunity and stress granule responses.

Author information

  • 1Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba 260-8673, Japan.
  • 2University of British Columbia (UBC) James Hogg Research Center, Providence Heart and Lung Institute, St. Paul's Hospital and Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada.
  • 3Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan; Laboratory of Molecular Cell Biology, Graduate School of Biostudies, Kyoto University, Kyoto 606-8507, Japan.
  • 4Laboratory of Molecular Genetics, Institute for Virus Research, Kyoto University, Kyoto 606-8507, Japan; Laboratory of Molecular Cell Biology, Graduate School of Biostudies, Kyoto University, Kyoto 606-8507, Japan. Electronic address: tfujita@virus.kyoto-u.ac.jp.

Abstract

Viral infection triggers the activation of antiviral innate immune responses in mammalian cells. Viral RNA in the cytoplasm activates signaling pathways that result in the production of interferons (IFNs) and IFN-stimulated genes. Some viral infections have been shown to induce cytoplasmic granular aggregates similar to the dynamic ribonucleoprotein aggregates termed stress granules (SGs), suggesting that these viruses may utilize this stress response for their own benefit. By contrast, some viruses actively inhibit SG formation, suggesting an antiviral function for these structures. We review here the relationship between different viral infections and SG formation. We examine the evidence for antiviral functions for SGs and highlight important areas of inquiry towards understanding cellular stress responses to viral infection.

KEYWORDS:

dsRNA; innate immunity; interferon; shut-off; stress granules; virus infection

PMID:
25153707
DOI:
10.1016/j.it.2014.07.006
[PubMed - indexed for MEDLINE]
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