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Antiviral innate immunity and stress granule responses

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...

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Detalles Bibliográficos
Autores principales: Onomoto, Koji, Yoneyama, Mitsutoshi, Fung, Gabriel, Kato, Hiroki, Fujita, Takashi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Published by Elsevier Ltd. 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185371/
https://www.ncbi.nlm.nih.gov/pubmed/25153707
http://dx.doi.org/10.1016/j.it.2014.07.006
Descripción
Sumario: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.