Publications
2014
Chtarbanova Stanislava, Lamiable Olivier, Lee Kwang-Zin, Galiana Delphine, Troxler Laurent, Meignin Carine, Hetru Charles, Hoffmann Jules A, Daeffler Laurent, Imler Jean-Luc
Drosophila C virus systemic infection leads to intestinal obstruction Article de journal
Dans: Journal of Virology, vol. 88, no. 24, p. 14057–14069, 2014, ISSN: 1098-5514.
Résumé | Liens | BibTeX | Étiquettes: Animals, bioinformatic, Dicistroviridae, Female, Gastrointestinal Tract, Gene Expression Profiling, hoffmann, imler, Intestinal Obstruction, M3i, meignin, Muscle, Nodaviridae, Sindbis Virus, Smooth, Viral Tropism
@article{chtarbanova_drosophila_2014,
title = {Drosophila C virus systemic infection leads to intestinal obstruction},
author = {Stanislava Chtarbanova and Olivier Lamiable and Kwang-Zin Lee and Delphine Galiana and Laurent Troxler and Carine Meignin and Charles Hetru and Jules A Hoffmann and Laurent Daeffler and Jean-Luc Imler},
url = {http://jvi.asm.org/content/88/24/14057},
doi = {10.1128/JVI.02320-14},
issn = {1098-5514},
year = {2014},
date = {2014-12-01},
journal = {Journal of Virology},
volume = {88},
number = {24},
pages = {14057--14069},
abstract = {Drosophila C virus (DCV) is a positive-sense RNA virus belonging to the Dicistroviridae family. This natural pathogen of the model organism Drosophila melanogaster is commonly used to investigate antiviral host defense in flies, which involves both RNA interference and inducible responses. Although lethality is used routinely as a readout for the efficiency of the antiviral immune response in these studies, virus-induced pathologies in flies still are poorly understood. Here, we characterize the pathogenesis associated with systemic DCV infection. Comparison of the transcriptome of flies infected with DCV or two other positive-sense RNA viruses, Flock House virus and Sindbis virus, reveals that DCV infection, unlike those of the other two viruses, represses the expression of a large number of genes. Several of these genes are expressed specifically in the midgut and also are repressed by starvation. We show that systemic DCV infection triggers a nutritional stress in Drosophila which results from intestinal obstruction with the accumulation of peritrophic matrix at the entry of the midgut and the accumulation of the food ingested in the crop, a blind muscular food storage organ. The related virus cricket paralysis virus (CrPV), which efficiently grows in Drosophila, does not trigger this pathology. We show that DCV, but not CrPV, infects the smooth muscles surrounding the crop, causing extensive cytopathology and strongly reducing the rate of contractions. We conclude that the pathogenesis associated with systemic DCV infection results from the tropism of the virus for an important organ within the foregut of dipteran insects, the crop. IMPORTANCE: DCV is one of the few identified natural viral pathogens affecting the model organism Drosophila melanogaster. As such, it is an important virus for the deciphering of host-virus interactions in insects. We characterize here the pathogenesis associated with DCV infection in flies and show that it results from the tropism of the virus for an essential but poorly characterized organ in the digestive tract, the crop. Our results may have relevance for other members of the Dicistroviridae, some of which are pathogenic to beneficial or pest insect species.},
keywords = {Animals, bioinformatic, Dicistroviridae, Female, Gastrointestinal Tract, Gene Expression Profiling, hoffmann, imler, Intestinal Obstruction, M3i, meignin, Muscle, Nodaviridae, Sindbis Virus, Smooth, Viral Tropism},
pubstate = {published},
tppubtype = {article}
}
Lestradet Matthieu, Lee Kwan Zin, Ferrandon Dominique
Drosophila as a model for intestinal infections Article de journal
Dans: Methods Mol Biol, vol. 1197, p. 11–40, 2014, ISSN: 1940-6029 (Electronic) 1064-3745 (Linking).
Résumé | Liens | BibTeX | Étiquettes: Animal, Animals, Bacterial Physiological Phenomena, Disease Models, ferrandon, Gastrointestinal Tract, Host-Pathogen Interactions, M3i
@article{lestradet_drosophila_2014b,
title = {Drosophila as a model for intestinal infections},
author = {Matthieu Lestradet and Kwan Zin Lee and Dominique Ferrandon},
doi = {10.1007/978-1-4939-1261-2_2},
issn = {1940-6029 (Electronic) 1064-3745 (Linking)},
year = {2014},
date = {2014-01-01},
journal = {Methods Mol Biol},
volume = {1197},
pages = {11--40},
abstract = {Drosophila melanogaster is a powerful model to study infections thanks to the power of its genetics and knowledge on its biology accumulated for over a century. While the systemic humoral immune response against invading microbes has been intensively studied in the past two decades, the study of intestinal infections is more recent. Here, we present the methods that are currently in use to probe various aspects of the host-pathogen interactions between Drosophila and ingested microbes, with an emphasis on the study of the midgut epithelium, which constitutes the major interface between the organism and the microbe-rich ingested food.},
keywords = {Animal, Animals, Bacterial Physiological Phenomena, Disease Models, ferrandon, Gastrointestinal Tract, Host-Pathogen Interactions, M3i},
pubstate = {published},
tppubtype = {article}
}
2006
Shiao Shin-Hong, Whitten Miranda M A, Zachary Daniel, Hoffmann Jules A, Levashina Elena A
Fz2 and cdc42 mediate melanization and actin polymerization but are dispensable for Plasmodium killing in the mosquito midgut Article de journal
Dans: PLoS Pathog., vol. 2, no. 12, p. e133, 2006, ISSN: 1553-7374.
Résumé | Liens | BibTeX | Étiquettes: Actins, Animals, Anopheles, Carrier Proteins, cdc42 GTP-Binding Protein, Double-Stranded, Electron, Frizzled Receptors, Gastrointestinal Tract, hoffmann, Host-Parasite Interactions, Immunity, Innate, Insect Vectors, Intestinal Mucosa, M3i, Melanins, Microarray Analysis, Microscopy, Plasmodium berghei, Polymers, Protozoan, RNA, scanning, telomerase
@article{shiao_fz2_2006,
title = {Fz2 and cdc42 mediate melanization and actin polymerization but are dispensable for Plasmodium killing in the mosquito midgut},
author = {Shin-Hong Shiao and Miranda M A Whitten and Daniel Zachary and Jules A Hoffmann and Elena A Levashina},
doi = {10.1371/journal.ppat.0020133},
issn = {1553-7374},
year = {2006},
date = {2006-12-01},
journal = {PLoS Pathog.},
volume = {2},
number = {12},
pages = {e133},
abstract = {The midgut epithelium of the mosquito malaria vector Anopheles is a hostile environment for Plasmodium, with most parasites succumbing to host defenses. This study addresses morphological and ultrastructural features associated with Plasmodium berghei ookinete invasion in Anopheles gambiae midguts to define the sites and possible mechanisms of parasite killing. We show by transmission electron microscopy and immunofluorescence that the majority of ookinetes are killed in the extracellular space. Dead or dying ookinetes are surrounded by a polymerized actin zone formed within the basal cytoplasm of adjacent host epithelial cells. In refractory strain mosquitoes, we found that formation of this zone is strongly linked to prophenoloxidase activation leading to melanization. Furthermore, we identify two factors controlling both phenomena: the transmembrane receptor frizzled-2 and the guanosine triphosphate-binding protein cell division cycle 42. However, the disruption of actin polymerization and melanization by double-stranded RNA inhibition did not affect ookinete survival. Our results separate the mechanisms of parasite killing from subsequent reactions manifested by actin polymerization and prophenoloxidase activation in the A. gambiae-P. berghei model. These latter processes are reminiscent of wound healing in other organisms, and we propose that they represent a form of wound-healing response directed towards a moribund ookinete, which is perceived as damaged tissue.},
keywords = {Actins, Animals, Anopheles, Carrier Proteins, cdc42 GTP-Binding Protein, Double-Stranded, Electron, Frizzled Receptors, Gastrointestinal Tract, hoffmann, Host-Parasite Interactions, Immunity, Innate, Insect Vectors, Intestinal Mucosa, M3i, Melanins, Microarray Analysis, Microscopy, Plasmodium berghei, Polymers, Protozoan, RNA, scanning, telomerase},
pubstate = {published},
tppubtype = {article}
}