Pathogen intrusion triggers an immediate host response leading in most cases to the elimination of the microbe. Type-I interferons (IFN-alpha/beta) 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-kappa B transcription factors which drive the synthesis of IFN-alpha/beta 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 propel-ties. However, viruses have evolved diverse strategies to escape the IFN response.
Viruses and interferon: mechanisms of interferon induction and strategies to escape interferon response
Bouttier, M.; Goncalves, C.; Journo, C.; Letienne, J.; Pina, M.; Vitour, D.
2008-06 / vol 12 / pages 159-173
IGMM team(s) involved in this publication
virus; nf-kappa-b; interferon; activated protein-kinase; alpha/beta-interferon; antiviral responses; double-stranded-rna; hepatitis-c virus; influenza-a-virus; innate immune-response; innate immunity; rig-i; rig-i/mda5 helicases; toll-like receptor; toll-like receptor-3