Classical swine fever virus (CSFV) is capable of counteracting innate cellular antiviral responses by inhibiting type I interferon (IFN)-alpha/beta induction. A function associated with CSFV N(pro), with respect to the inhibition of IFN-beta production, has been clearly elucidated. In this study, we explored the role of CSFV E(rns) in IFN-beta induction by exogenous double-stranded (ds) RNA. Synthetic dsRNA (poly (IC)) was used as an exogenous stimulus to trigger IFN-beta induction. CSFV E(rns) inhibited IFN-beta promoter-driven luciferase activity induced by poly (IC) in different cell lines, and the inhibitory effect was dose-dependent. Moreover, E(rns) reduced IFN-beta mRNA synthesis and blocked IFN-alpha/beta production induced by poly (IC), suggesting that this inhibition occurs at the transcriptional level. Furthermore, E(rns) counteracted poly (IC)-mediated IFN-beta induction independent of its ribonuclease activity. In conclusion, CSFV E(rns) antagonizes extracellular dsRNA-mediated IFN-beta expression. These findings contribute to our understanding of the pathogenesis of CSFV.