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Cricket Paralysis Virus (CrPV) antagonizes Argonaute 2 to modulate antiviral defense in Drosophila

Insect viruses have evolved strategies to control the host RNAi antiviral defense mechanism. In nature Drosophila C Virus (DCV) infection causes low mortality and persistent infection, whereas the closely related Cricket Paralysis Virus (CrPV) causes a lethal infection. We show these viruses use dif...

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Detalles Bibliográficos
Autores principales: Nayak, Arabinda, Berry, Bassam, Tassetto, Michel, Kunitomi, Mark, Acevedo, Ashley, Deng, Changhui, Kruchinsky, Andrew, Gross, John, Antoniewski, Christophe, Andino, Raul
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815677/
https://www.ncbi.nlm.nih.gov/pubmed/20400949
http://dx.doi.org/10.1038/nsmb.1810
Descripción
Sumario:Insect viruses have evolved strategies to control the host RNAi antiviral defense mechanism. In nature Drosophila C Virus (DCV) infection causes low mortality and persistent infection, whereas the closely related Cricket Paralysis Virus (CrPV) causes a lethal infection. We show these viruses use different strategies to modulate the host RNAi defense machinery. The DCV RNAi suppressor (DCV-1A) binds to long double-stranded RNA (dsRNA) and prevents processing by Dicer2. In contrast, the CrPV suppressor (CrPV-1A) interacts with the endonuclease Ago2 and inhibits its activity, without affecting the miRNA-Ago1 mediated silencing. The link between viral RNAi suppressors and the outcome of infection was examined using recombinant Sindbis viruses encoding either CrPV-1A or DCV-1A. Flies infected with Sindbis virus expressing CrPV-1A showed a dramatic 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.