Abstract
The innate immune response is the major front line of defense against viral infections. It involves hundreds of genes with antiviral properties which expression is induced by type I interferons (IFNs) and are therefore called interferon stimulated genes (ISGs). Type I IFNs are produced after viral recognition by pathogen recognition receptors, which trigger a cascade of activation events. Human and mouse studies have shown that defective type I IFNs induction may hamper the ability to control viral infections. In humans, moderate to high-effect variants have been identified in individuals with particularly severe complications following viral infection. In mice, functional studies using knock-out alleles have revealed the specific role of most genes of the IFN pathway. Here, we review the role of the molecular partners of the type I IFNs induction pathway and their implication in the control of viral infections and of their complications.
【초록키워드】 viral infection, innate immune response, Human, variant, interferon, viral infections, type I interferon, pathogen, mice, humans, complications, IFN, receptors, molecular, expression, moderate, ISGs, IFNs, antiviral property, Type I IFN, Activation, individual, allele, cascade, Defense, knock-out, IFN pathway, stimulated, produced, shown, events, functional, Type, severe complication, induction pathway, 【제목키워드】 type I interferon, genetic susceptibility,