RNAi-Based Antiviral Innate Immunity in Plants

Abstract

Multiple antiviral immunities were developed to defend against viral infection in hosts. RNA interference (RNAi)-based antiviral innate immunity is evolutionarily conserved in eukaryotes and plays a vital role against all types of viruses. During the arms race between the host and virus, many viruses evolve viral suppressors of RNA silencing (VSRs) to inhibit antiviral innate immunity. Here, we reviewed the mechanism at different stages in RNAi-based antiviral innate immunity in plants and the counteractions of various VSRs, mainly upon infection of RNA viruses in model plant Arabidopsis. Some critical challenges in the field were also proposed, and we think that further elucidating conserved antiviral innate immunity may convey a broad spectrum of antiviral strategies to prevent viral diseases in the future.

Keywords: RNAi; VSR; antiviral innate immunity; small RNA; virus.

Figure 1

RNAi-based antiviral pathway in model plant Arabidopsis. After viral infection, the double-stranded viral RNA replicate intermediate will be perceived and processed into 21, 22, or 24 nt duplex primary viral siRNAs, respectively, by DCL4, DCL2, or DCL3. These 21 and 22nt primary viral siRNAs will then be uploaded into AGO1 or AGO2 to form RISC to mediate the slicing or translation inhibition of RNA viruses through PTGS. In contrast, 24nt vsiRNA will be uploaded to AGO4, AGO6, or AGO9 to form RISC to induce DNA methylation or histone modification through TGS to silence DNA viruses. Secondary viral siRNAs produced through amplification by RDR1/RDR6 or RDR2 are, respectively, required to enforce RNAi-based antiviral defense against RNA viruses or DNA viruses. Various VSRs of plant viruses target different steps to inhibit antiviral immunity.

Figure 2

Protein structure diagram of DCLs, AGOs, RDRs, and ALAs. Function domains of each protein are shown with different colored boxes.