Author: Stanislava ChtarbanovaPublisher:
ISBN:
Category :
Languages : en
Pages : 320
Book Description
Insects are exposed in their environement to many viruses, and these infections can have a significant economic or medical impact. At present, little is known about the pathophysiological mechanisms involved in susceptibility to viral infections. We used the model organism Drosophila melanogaster to study the pathology induced by two RNA viruses: the Drosophila C virus (DCV) and the Flock House Virus (FHV).We compared the transcriptome of DCV and FHV-infected flies by using genome-wide microarrays. DCV infection leads to the strong repression of several hundred of genes, mainly expressed in the midgut of the fly. Many genes repressed by the DCV are also repressed under conditions of starvation, suggesting that infected flies stop feeding. However, DCV-infected flies continue to feed and gain weight until their death. This is due to decreased excretion, associated with an intestinal obstruction in the anterior midgut of the fly that probably occurs at the level of the cardia. The pathology induced by DCV results from the presence of the virus in a particular tissue, rather than from the adverse effect of the host's immune response. On the other hand, we identified the gene dSUR, which encode the subunit of an ATP-dependent potassium channel (KATP). dSUR is expressed in the Drosophila heart and mutants for this gene are more sensitive to FHV and contain higher viral loads than controls. We showed that FHV is cardiotropic virus and that the cardiac KATP activity is related to the major antiviral mechanism RNA interference. Our work shows that DCV and FHV, which appear very similar at first sight, induce very different, organ-specific pathologies in Drosophila.
