Rice stripe virus NS3 uses the host signaling pathways to control pathogenicity.

Viruses pose a significant threat to animal and plant health worldwide. How viruses adapt to vectors and hosts more sustainably remains unclear. Rice stripe virus (RSV) is a devastating rice-infecting RNA virus and is exclusively transmitted by Laodelphax striatellus (Fallén). During the early stages of viral infection, limited NS3 protein undergoes self-interaction, thereby suppressing the host's antiviral RNA interference (RNAi) pathway. Meanwhile, RSV-induced Ca2+ signals activate the OsSnRK3.25-OsCBL1/3-OsRBOHs-mediated reactive oxygen species (ROS) burst and programmed cell death (PCD). RSV exhibits strong pathogenicity and transmissibility. In later stages, an abundance of NS3 interacts with OsSnRK3.25 and undergoes phosphorylation, which enhances the host antiviral RNAi pathway while concurrently disrupting the endogenous OsSnRK3.25-OsCBL1/3-OsRBOHs signaling. Here, RSV demonstrates reduced pathogenicity and transmissibility. Thus, the virus fine-tunes its pathogenicity and transmissibility by NS3 phosphorylation and hijacking OsSnRK3.25, sustaining a delicate balance between virus-host-vector interactions. This study identifies a co-survival strategy within virus-vector-host triple interactions.