Nature Immunology 7, 590 - 597 (2006)
Published online: 23 March 2006; | doi:10.1038/ni1335
Essential function in vivo for Dicer-2 in host defense against RNA viruses in drosophilaDelphine Galiana-Arnoux1, 3, Catherine Dostert1, 3, Anette Schneemann2, Jules A Hoffmann1
& Jean-Luc Imler11
UPR9022 Centre National de la Recherche Scientifique, Institut de Biologie Moléculaire et Cellulaire Strasbourg 67000, France. 2
Department of Molecular Biology, The Scripps Research Institute, La Jolla, California 92037, USA. 3
These authors contributed equally to this study.
Correspondence should be addressed to Jean-Luc Imler jl.imler@ibmc.u-strasbg.fr The fruit fly Drosophila melanogaster is a model system for studying innate immunity, including antiviral host defense. Infection with drosophila C virus triggers a transcriptional response that is dependent in part on the Jak kinase Hopscotch. Here we show that successful infection and killing of drosophila with the insect nodavirus flock house virus was strictly dependent on expression of the viral protein B2, a potent inhibitor of processing of double-stranded RNA mediated by the essential RNA interference factor Dicer. Conversely, flies with a loss-of-function mutation in the gene encoding Dicer-2 (Dcr-2) showed enhanced susceptibility to infection by flock house virus, drosophila C virus and Sindbis virus, members of three different families of RNA viruses. These data demonstrate the importance of RNA interference for controlling virus replication in vivo and establish Dcr-2 as a host susceptibility locus for virus infections.
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