Fig. 2

The antiviral RNA silencing model and VSRs with diverse sets of strategies for battling against RNA silencing [adapted from Burgyán and Havelda (2011), Csorba et al. (2015), Gaffar and Koch (2019)]. An antiviral response is initiated with the biogenesis of 21–24 nt vsiRNAs and miRNAs, the silencing molecules that are produced through DCL processing (vsiRNAs are produced primarily by DCL4 and secondarily by DCL2 in the cytoplasm, whereas miRNAs are synthesized in the nucleus by DCL1). These silencing molecules are stabilized by the HEN1 methylation process and subsequently loaded into AGOs to form an RNA-induced silencing complex (RISC), followed by the effector phase of post-transcriptional gene silencing (PTGS) completed through viral RNA cleavage or translational inhibition. To amplify the antiviral RNA silencing response, AGO-sliced products and aberrant viral transcripts or RNAs are used as templates for RDR complexes employing RNA-helicases (SGS3 and SDE5), the cofactors of RDRs triggered pathways. Transcriptional gene silencing (TGS) is triggered by the production of 24-nt vsiRNAs via DCL3 processing (nucleus) in the case of DNA virus infection. HEN1-methylated 24-nt vsiRNAs are loaded into AGO4 to complete TGS after methylation of the viral genome through a DNA methylation cycle mediated by Pol II, ADK, SAHH, and SAMS. VSRs that interfere with PTGS or TGS are presented in boxes along the sides of the figure. The lines indicate the target site at which VSRs interact with the antiviral pathway