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.

先天免疫反应是抵御病毒感染的主要前线。它涉及数百个具有抗病毒特性的基因，其表达由 I 型干扰素 (IFN) 诱导，因此被称为干扰素刺激基因 (ISG)。I 型干扰素是在病毒识别后由病原体识别受体产生的，这会触发一连串的激活事件。人类和小鼠研究表明，有缺陷的 I 型干扰素诱导可能会妨碍控制病毒感染的能力。在人类中，已在病毒感染后出现特别严重并发症的个体中鉴定出中度至高效变异体。在小鼠中，使用敲除等位基因的功能研究揭示了 IFN 通路中大多数基因的特定作用。这里，