Viral proteins resolve the virus-vector conundrum during hemipteran-mediated transmission by subverting salicylic acid signaling pathway

Hemipteran insects transmit viruses when infesting plants, during which vectors activate salicylic acid (SA)-regulated antiviral defenses. How vector-borne plant viruses circumvent these antiviral defenses is largely unexplored. During co-infections of begomoviruses and betasatellite-encoded βC1 proteins interfere with SA signaling and reduce the activation of antiviral resistance. βC1 inhibits SA-induced degradation of NbNPR3 (Nicotiana benthamiana nonexpresser of PR genes 3), a negative regulator of SA signaling. βC1 does not bind directly to NbNPR3, but NbNPR3 degradation via heat shock protein 90 (NbHSP90s) binds to both NbNPR3 and βC1 and suppress SA signaling. This viral rescue strategy appears to be conserved as it is also documented for viral proteins encoded by two aphid-borne viruses. Our findings reveal an exquisite mechanism that facilitates the persistence of vector-borne viruses and provide important insights into the intricacies of the virus life cycle.