西亚试剂：Antiviral immunity in Drosophila requires systemic RNA inte

Antiviral immunity in Drosophila requires systemic RNA interference spread

Maria-Carla Saleh1,4, Michel Tassetto1,5, Ronald P. van Rij1,5,4, Bertsy Goic2, Valérie Gausson2, Bassam Berry3, Caroline Jacquier3, Christophe Antoniewski3 & Raul Andino1

1 Department of Microbiology and Immunology, University of California, San Francisco 94122-2280, USA
2 Institut Pasteur, Viruses and RNA interference, F-75015 Paris, France
3 Institut Pasteur, Drosophila Genetics and  CNRS, URA 2578, F-75015 Paris, France
4 Present addresses: Institut Pasteur, Viruses and RNA interference, F-75015 Paris, France (M.-C.S.); Department of Medical Microbiology, Nijmegen Center for Molecular Life Sciences, University Medical Center 5 Nijmegen, PO Box 9101, 6500 HB Nijmegen, The Netherlands (R.P.v.R.).
6 These authors contributed equally to this work.
7 Correspondence to: Raul Andino1 Correspondence and requests for materials should be addressed to R.A.

Multicellular organisms evolved sophisticated defence systems to confer protection against pathogens. An important characteristic of these immune systems is their ability to act both locally at the site of infection and at distal uninfected locations1, 2, 3, 4. In insects, such as Drosophila melanogaster, RNA interference (RNAi) mediates antiviral immunity5, 6, 7. However, the antiviral RNAi defence in flies seems to be a local, cell-autonomous process, as flies are thought to be unable to generate a systemic RNAi response8. Here we show that a recently defined double-stranded RNA (dsRNA) uptake pathway9 is essential for effective antiviral RNAi immunity in adult flies. Mutant flies defective in this dsRNA uptake pathway were hypersensitive to infection with Drosophila C virus and Sindbis virus. Mortality in dsRNA-uptake-defective flies was accompanied by 100-to 105-fold increases in viral titres and higher levels of viral RNA. Furthermore, inoculating naked dsRNA into flies elicited a sequence-specific antiviral immune response that required an intact dsRNA uptake pathway. These findings suggest that spread of dsRNA to uninfected sites is essential for effective antiviral immunity. Notably, infection with green fluorescent protein (GFP)-tagged Sindbis virus suppressed expression of host-encoded GFP at a distal site. Thus, similar to protein-based immunity in vertebrates, the antiviral RNAi response in

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