Bluetongue virus (BTV), a member of the orbivirus genus of the family Reoviridae, is an arthropod-borne pathogen of ruminants. This virus can cause up to 70 per cent mortality in sheep breeds which are particularly susceptible. Therefore bluetongue disease (BT) is a considerable socioeconomic concern causing limitations on international trade of animals during outbreaks. Due to the lack of a reverse genetic model for this dsRNA virus until recently, the molecular mechanisms that govern the viral pathogenesis have remained poorly investigated. In 70’s and 80’s, some works have showed that BTV genomic dsRNA can induce the production of type-I interferon (IFN-I). However nothing is known about underlying mechanisms involved in this process. In a kinetic study, we showed that BTV serotype 8, isolated during the outbreak in France in 2006, can trigger IFN-I synthesis in human epithelial cells (A549) at the mRNA and protein level. We also demonstrated that a number of inflammatory cytokines and IFN-stimulated genes are upregulated during infection. Moreover a UV-inactivated virus doesn’t trigger the production of IFN-?, implying that replication is necessary for the IFN-I production. Now we are addressing the question of viral attenuation on cytokine production. We also confirmed that purified genomic dsRNA, from BTV8 origin, activate IFN production. Using siRNA knockdown, we demonstrated that BTV-8 dsRNA use the RIG-like receptor pathway to trigger the activation of IFN-? promoter. Now we want to investigate this question at the virus level and to assess the involvement of other dsRNA sensors like TLR3 or PKR. Afterwards these results will be confirmed in primary ovine endothelial cells.