Virologie
MENUViruses and interferon : mechanisms of interferon induction and strategies to escape interferon response Volume 12, issue 3, Mai-Juin 2008
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- Key words: virus, innate immunity, interferon, Toll-like receptor, RIG-I/MDA5 helicases
- DOI : 10.1684/vir.2008.0173
- Page(s) : 159-73
- Published in: 2008
Pathogen intrusion triggers an immediate host response leading in most cases to the elimination of the microbe. Type-I interferons (IFN-α/β) 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-κB transcription factors which drive the synthesis of IFN-α/β 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.