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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.
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10.1038/s41435-020-00116-2
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document_parses/pdf_json/51ea5073c9b4f29492b9b2148a486a4b1f5c9d74.json
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document_parses/pmc_json/PMC7677911.xml.json
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Host genetic susceptibility to viral infections: the role of type I interferon induction
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