The Toll-Dorsal Pathway Is Required for Resistance to Viral Oral Infection in Drosophila

Abstract

Pathogen entry route can have a strong impact on the result of microbial infections in different hosts, including insects. Drosophila melanogaster has been a successful model system to study the immune response to systemic viral infection. Here we investigate the role of the Toll pathway in resistance to oral viral infection in D. melanogaster. We show that several Toll pathway components, including Spätzle, Toll, Pelle and the NF-kB-like transcription factor Dorsal, are required to resist oral infection with Drosophila C virus. Furthermore, in the fat body Dorsal is translocated from the cytoplasm to the nucleus and a Toll pathway target gene reporter is upregulated in response to Drosophila C Virus infection. This pathway also mediates resistance to several other RNA viruses (Cricket paralysis virus, Flock House virus, and Nora virus). Compared with control, viral titres are highly increased in Toll pathway mutants. The role of the Toll pathway in resistance to viruses in D. melanogaster is restricted to oral infection since we do not observe a phenotype associated with systemic infection. We also show that Wolbachia and other Drosophila-associated microbiota do not interact with the Toll pathway-mediated resistance to oral infection. We therefore identify the Toll pathway as a new general inducible pathway that mediates strong resistance to viruses with a route-specific role. These results contribute to a better understanding of viral oral infection resistance in insects, which is particularly relevant in the context of transmission of arboviruses by insect vectors.

Transcriptional signatures of parasitization and markers of colony decline in Varroa-infested honey bees (Apis mellifera)

“…The role of this gene in antiviral defence has been supported by a study showing that a treatment with the neonicotinoid insecticide clothianidin, that indirectly targets the same gene, results in high levels of DWV replication (Di Prisco et al, 2013). Interestingly, the role of dorsal in antiviral defence does not seem to be restricted to honey bees, since it has been shown that the Toll-Dorsal Pathway is required for resistance to viral oral infection in the fruit fly as well (Ferreira et al, 2014). The observed effect on dorsal appears to be particularly interesting in view of the increased viral infection in mite infested bees confirmed in this study.…”

Protection of Insects against Viral Infection by Apoptosis-Dependent Phagocytosis

“…However, it remains to be determined how flies succumb to DCV infection. DCV infects a variety of tissues and organs in Drosophila, including the fat body, periovarial sheath, trachea, muscle, and digestive tract (31,44,62,67,68). A recent report argued that alteration in a variety of physiological and metabolic phenomena is related to the death of DCV-infected flies (69).…”

“…Recent studies reported changes in the morphology of flies (i.e., abdominal swelling and crop enlargement) upon infection with DCV (31,62). We wondered whether such morphological changes are due to the expansion of infection.…”

“…We focused on this issue using Drosophila C virus (DCV), a nonenveloped positive-strand RNA virus assigned to the Dicistroviridae genus Cripavirus, which has been recognized as a natural pathogen of Drosophila (27,28). Previous studies showed the existence of several modes of antiviral immunity activated in Drosophila upon infection with DCV, which involve RNAi (11,29,30), the Toll-Dorsal pathway (31), and the JAK-STAT pathway (32). All of these mechanisms use humoral immune reactions.…”

Protective effects of <i>Phaseolus vulgaris</i> lectin against viral infection in <i>Drosophila </i>

“…Both humoral (23) and cellular (19) immunity play roles in the protection of flies against viral infection, including that with DCV. Therefore, we compared the amounts of the mRNAs of antimicrobial peptides and Hours post-infection when flies start to die (onset) and all flies are dead (extinct) are shown as a summary of the data from three independent experiments with two different viral doses.…”