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Updated: Aug 28, 2025

Dissecting Innate Immune Signaling in Viral Evasion of Cytokine Production
Published on: March 2, 2014
[Viruses and interferon: mechanisms of interferon induction and strategies to escape interferon response]
M Bouttier1, C Goncalvès2, C Journo3
1UMR 5535 Institut de génétique moléculaire de Montpellier, Centre national de la recherche scientifique, 1919, route de Mende, 34293 Montpellier Cedex 5.
Abstract:
Pathogen intrusion triggers an immediate host response leading in most cases to the elimination of the microbe. Type-I interferons (IFN-a/b) production and release is a major event in innate antiviral immunity through the establishment of an antiviral state in neighbouring cells. IFN production depends on the interaction between viral PAMPs (pathogen-associated molecular patterns) and their corresponding cellular sensors-also called PRRs (pattern recognition receptors)-either from membranous (Toll-like receptors) or cytosolic (RIG-I helicase) origin. Activated PRRs can recruit downstream partners in order to activate the IRF-3/7, AP1 and NF-jB transcription factors which drive the synthesis of IFN-a/b and inflammatory cytokines. Following binding to their cognate receptor, they activate a signaling cascade (Jak/STAT pathway) that leads to the synthesis of proteins endowed with antiviral or immunomodulatory properties. However, viruses have evolved diverse strategies to escape the IFN response.
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