Fiche publication


Date publication

juin 2016

Journal

Journal of virology

Auteurs

Membres identifiés du Cancéropôle Est :
Pr IMLER Jean-Luc , Dr MEIGNIN Carine


Tous les auteurs :
Lamiable O, Arnold J, de Faria IJDS, Olmo RP, Bergami F, Meignin C, Hoffmann JA, Marques JT, Imler JL

Résumé

Antiviral immunity in the model organism Drosophila melanogaster involves the broadly active intrinsic mechanism of RNA interference (RNAi) and virus-specific inducible responses. Here, using a panel of six viruses, we investigated the role of hemocytes and autophagy in the control of viral infections. Injection of latex beads to saturate phagocytosis, or genetic depletion of hemocytes, resulted in decreased survival and increased viral titers following infection with Cricket paralysis virus (CrPV), Flock House virus (FHV), and vesicular stomatitis virus (VSV) but had no impact on Drosophila C virus (DCV), Sindbis virus (SINV), and Invertebrate iridescent virus 6 (IIV6) infection. In the cases of CrPV and FHV, apoptosis was induced in infected cells, which were phagocytosed by hemocytes. In contrast, VSV did not trigger any significant apoptosis but we confirmed that the autophagy gene Atg7 was required for full virus resistance, suggesting that hemocytes use autophagy to recognize the virus. However, this recognition does not depend on the Toll-7 receptor. Autophagy had no impact on DCV, CrPV, SINV, or IIV6 infection and was required for replication of the sixth virus, FHV. Even in the case of VSV, the increases in titers were modest in Atg7 mutant flies, suggesting that autophagy does not play a major role in antiviral immunity in Drosophila Altogether, our results indicate that, while autophagy plays a minor role, phagocytosis contributes to virus-specific immune responses in insects.

Mots clés

Animals, Apoptosis, Autophagy, Autophagy-Related Protein 7, genetics, Cell Line, DNA Viruses, immunology, Drosophila, cytology, Drosophila Proteins, genetics, Hemocytes, immunology, Phagocytosis, RNA Interference, RNA Viruses, immunology, Sindbis Virus, immunology, Vesicular stomatitis Indiana virus, immunology, Virus Replication

Référence

J. Virol.. 2016 06 1;90(11):5415-5426