Virus-induced gene silencing (VIGS) is a common reverse genetics strategy for characterizing the function of genes in plants. The detailed mechanism governing RNA silencing efficiency triggered by viruses is largely unclear. Here, we reveal that a petunia (Petunia hybrida) ocs element binding factor,PhOBF1, one of the basic leucine zipper (bZIP) transcription factors, was up-regulated byTobacco rattle virus(TRV) infection. Simultaneous silencing ofPhOBF1and a reporter gene,phytoene desaturase(PDS) orchalcone synthase(CHS), by TRV-based VIGS led to a failure of the development of leaf photobleaching or the white-corollas phenotype.PhOBF1silencing caused down-regulation of RNA silencing-related genes, includingRNA-dependent RNA polymerases(RDRs),Dicer-like RNase III enzymes(DCLs), andArgonautes(AGOs). After inoculation with the TRV-PhPDS,PhOBF1-RNAi lines exhibited a substantially impairedPDSsilencing efficiency, whereas overexpression ofPhOBF1resulted in a recovery of the silencing phenotype (photobleaching) in systemic leaves. A compromised resistance to TRV andTobacco mosaic viruswas found inPhOBF1-RNAi lines, whilePhOBF1-overexpressing lines displayed an enhanced resistance to their infections. Compared with wild-type plants,PhOBF1-silenced plants accumulated lower levels of free salicylic acid (SA), salicylic acid glucoside, and phenylalanine, contrarily to higher levels of those in plants overexpressingPhOBF1. Furthermore, transcripts of a number of genes associated with the shikimate and phenylpropanoid pathways were decreased or increased inPhOBF1-RNAi orPhOBF1-overexpressing lines, respectively. Taken together, the data suggest that PhOBF1 regulates TRV-induced RNA silencing efficiency through modulation ofRDRs,DCLs, andAGOs mediated by the SA biosynthesis pathway.