当期论文

Evolutionary conflicts between viruses and hosts compel them to ceaselessly develop novel offense or defense strategies. Type I interferons (IFN) initiate robust intracellular antiviral programmes, representing the classic innate immunity in mammals. Nevertheless, pathogenic hantaviruses, especially Hantaan viruses (HTNV), might resoundingly evade IFN responses at late infection stage, the underlying mechanism of which remains opaque. In this issue, Si et al. demonstrated that HTNV infection blocked JAK/STAT signaling by activating the receptor-interacting protein kinase 3 (RIPK3), but not triggering necroptosis. RIPK3 ablation efficiently promoted the expression of IFN-stimulated genes (ISG) and restricted viral replication in vitro. RIPK3 knockout mice also acquired prompt HTNV clearance ability with strengthened systemic inflammatory responses. Further investigation indicated that RIPK3 interfered with IFN pathway by binding to and incapacitating STAT1 during late HTNV infection stage. The cover image illustrates the possible immune evasion process of HTNV by manipulating RIPK3 traps to impede STAT1-mediate antiviral effects (kindly designed and provided by Hongwei Ma, Fanglin Zhang, and Yingfeng Lei). See page 741-754 for details.