Journal
NATURE STRUCTURAL & MOLECULAR BIOLOGY
Volume 17, Issue 5, Pages 547-U41Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nsmb.1810
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Funding
- Pasteur Institute
- Centre National de la Recherche Scientifique
- Agence Nationale de la Recherche (AKROSS)
- Lebanese Centre National de la Recherche Scientifique
- US National Institutes of Health [AI40085, AI064738]
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Insect viruses have evolved strategies to control the host RNAi antiviral defense mechanism. In nature, Drosophila melanogaster C virus (DCV) infection causes low mortality and persistent infection, whereas the closely related cricket paralysis virus (CrPV) causes a lethal infection. We show that these viruses use different strategies to modulate the host RNAi defense machinery. The DCV RNAi suppressor (DCV-1A) binds to long double-stranded RNA and prevents processing by Dicer2. In contrast, the CrPV suppressor (CrPV-1A) interacts with the endonuclease Argonaute 2 (Ago2) and inhibits its activity without affecting the microRNA (miRNA)-Ago1-mediated silencing. We examined the link between viral RNAi suppressors and the outcome of infection using recombinant Sindbis viruses encoding either CrPV-1A or DCV-1A. Flies infected with Sindbis virus expressing CrPV-1A showed a marked increase in virus production, spread and mortality. In contrast, Sindbis pathogenesis was only modestly increased by expression of DCV-1A. We conclude that RNAi suppressors function as virulence factors in insects and can target the Drosophila RNAi pathway at different points.
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