RIGI and infection: Recently, using a recombinant SeVΔC, a mutant which lacks the SeV IFN antagonist protein C, our group found that in spite of growth conditions that normally inhibit DI genome accumulation, such as plaque purification and passaging at low multiplicity of infection, SeVΔC nevertheless contained a high amounts of DI RNAs and these molecules were again responsible for robust activation of RIG-I, stimulating IFN production [168].