Viral RNA factory formation and activation of antiviral innate immunity

通过细胞质中的RIG-I样受体(RLR)感知入侵的病毒RNA，并诱导抗病毒天然免疫，包括干扰素的产生。目前尚不清楚RLR感知病毒RNA的位置。我们发现，病毒感染诱导了RNA-蛋白质聚集体，RLR被招募到其中，并作为病毒RNS感知的平台。我们将这种聚集体称为抗病毒应激颗粒(AvSG)。我们还发现，几种病毒可以主动抑制avSG，以促进其复制。我们的发现还包括双链RNA传感器PKR和DHX36在avSG的形成中起着关键作用。

Invading viral RNA is sensed by RIG-I-like receptor (RLR) in the cytoplasm and antiviral innate immunity, including production of interferon, is induced. It was unclear where RLR senses viral RNA. We found that viral infection induces RNA-protein aggregates, in which RLR is recruited and acts as a platform for viral RNS sensing. We termed this aggregate as antiviral stress granule (avSG). We also found that several viruses actively inhibit avSG to facilitate their replication. Our findings also include that the double-stranded RNA sensors, PKR and DHX36 play critical roles in the formation of avSG.