Antiviral RNA-mediated silencing (RNAi) acts as a powerful innate immunity defence in plants, invertebrates and mammals. In C. elegans RNAi is systemic, i. e. RNAi silencing signals can move between cells and tissues. Furthermore RNAi effects can be inherited transgenerationally and may last for many generations. Neither the biological relevance of systemic RNAi nor transgenerational RNAi are currently understood. Here we examined the role of both pathways to protect C. elegans from viral infection. We studied the Orsay virus, a positive strand RNA virus related to Nodaviridiae, and the first and only virus known to infect C. elegans. We found that genes required for systemic or transgenerational RNAi did not have a role in antiviral defence. Furthermore, we found that Orsay virus infection did not elicit a systemic RNAi response even when a target for RNAi was provided using transgenes. Finally, we show that viral siRNAs, the effectors of RNAi, are not inherited to a level that provides any significant resistance to viral infection in the next generation. We conclude that systemic or transgenerational RNAi does not play a role in the defence to Orsay virus infection. Furthermore, our data suggest that there is a qualitative difference between experimental RNAi and antiviral RNAi. Our data are consistent with a model of systemic and transgenerational RNAi that requires a nuclear or germline component which is lacking in RNA virus infection.