Small interfering RNAs generated from the terminal panhandle structure of negative-strand RNA virus promote viral infection.

Virus-derived small interfering RNAs (vsiRNAs) have been widely recognized to play an antiviral immunity role. However, it is unclear whether vsiRNAs can also play a positive role in viral infection. Here, we characterized three highly abundant vsiRNAs mapped to the genomic termini of rice stripe virus (RSV), a negative-strand RNA virus transmitted by insect vectors. The three vsiRNAs shared 11 nucleotides due to the conservative genomic termini and were likely generated from viral terminal panhandle structure, depending on both Dicer1 and Dicer2 in insects. In addition to targeting viral RNAs in a miRNA-like manner, the three vsiRNAs coordinately downregulated the expression of DOPA decarboxylase, thereby suppressing the prophenoloxidase immune reaction in insect vectors. In vsiRNA-silenced transgenic rice, the viral titer significantly decreased, indicating that these vsiRNAs promote RSV replication in rice. This study elucidates a unique function of vsiRNAs derived from the conserved panhandle structure of negative-strand RNA viruses in enhancing viral infection. Author summary: RNA interference (RNAi) is one of the important innate immune systems against viruses in insects. Virus-derived small interfering RNAs (vsiRNAs) have been widely recognized to play an antiviral immunity role. Here, we find that three vsiRNAs generated from the terminal panhandle structure of a rice virus promote viral infection in both insect vectors and host plants. These vsiRNAs coordinately target DOPA decarboxylase to inhibit melanization immune reaction in insect vectors. The vsiRNA-silenced transgenic rice exhibits an antiviral phenotype. Our work reveals a conserved positive effect of vsiRNAs from negative-strand RNA viruses on viral infection. [ABSTRACT FROM AUTHOR]