Fig. 7. Proposed model.

NF-κB activation following TLR3, TNFR, or IL-1R stimulation or following RLR stimulation (not depicted) promotes pro-IL-1β expression (signal I). In parallel, after infection, RNA virus replicates into the cell triggering a lytic form of cell death and plasma membrane rupture. This lytic cell death allows K⁺ efflux (signal II) that activates NLRP3 inflammasome. Within this inflammasome, caspase-1 is activated then cleaves pro-IL-1β into its mature form. IL-1β is released in the extracellular medium independently of the gasdermin D pores, likely as a consequence of the viral-induced lytic cell death