Scheme summarizing the inhibitory effect of TSN on PRRSV replication via activation of caspase-1 and induced maturation of IL-1β in an IFI16-dependent pathway. TSN significantly upregulates IFI16 expression in Marc-145 cells and PAMs. During primary infection of Marc-145 cells or PAMs, PRRSV nucleocapsid travels to the nuclear pore, and the linear RNA enters the nucleus, which is sensed by IFI16 during latency. This leads to the recruitment of ASC and pro-caspase-1 to form an inflammasome complex; the complex subsequently translocates to the cytoplasm to activate caspase-1, which then catalyzes the maturation of IL-1β. Eventually, the activated IL-1β are sorted and released from cells to inhibit PRRSV.