dmel_VSV
RNAi mediated immunity provides strong protection against the negative strand RNA virus VSV in Drosophila
Dataset 1 described in the paper linked below. These data are co-released by the Virus and Rna Interference Lab at the Institut Pasteur, Paris, France and the Reaction Antivirale group at the Institut de Biologie Moleculaire et Cellulaire, Strasbourg, France
Activation of innate antiviral responses in multicellular organisms largely relies on the recognition of structural differences between viral and cellular RNAs. Double-stranded (ds) RNA, produced during viral replication, is a well-known activator of antiviral defenses and triggers interferon production in vertebrates and RNA interference (RNAi) in invertebrates and plants. Previous work in mammalian cells indicates that negative-strand RNA viruses do not appear to generate dsRNA, and that activation of innate immunity is triggered by the recognition of the viral RNA uncapped 5’ ends. Studies on antiviral RNAi in plants and insects have so far focused on viruses with (+) strand or dsRNA genomes, raising the question whether RNAi, which is triggered by dsRNA, represents an effective host-defense mechanism against (-) strand RNA viruses. Here, we show that the (-) strand RNA virus Vesicular Stomatitis virus (VSV) does not produce detectable amounts of dsRNA in drosophila cells. However, RNAi represents a potent response to VSV infection, as illustrated by the high susceptibility of RNAi defective mutant flies to this virus. VSV-derived small RNAs produced in infected cells or flies equally map the (+) and (-) viral RNA strands, and cover uniformly the viral genome, supporting their production from dsRNA. Our findings reveal that RNAi is not restricted to the defense against (+) strand or dsRNA viruses but can also be highly efficient against a (-) strand RNA virus. This is of particular interest in view of the frequent transmission of medically relevant (-) strand RNA viruses to humans by insect vectors.