Physiological and metabolic consequences of viral infection in <i>Drosophila melanogaster</i>

Arnold, Pieter A.; Johnson, Karyn N.; White, Craig R.

doi:10.1242/jeb.088138

Cited by 78 publications

(94 citation statements)

References 60 publications

(68 reference statements)

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“…ERK has a broad substrate range (Futran et al, 2013;Wortzel & Seger, 2011) and its activation can lead to many diverse impacts on cells and the organism. Clues to the cause of higher mortality for DCV-infected ERK(À) flies may come from the pathology caused by DCV infection and may involve a combination of physiological- (Arnold et al, 2013;Chtarbanova et al, 2014) and host immunity- (Xu et al, 2013) related factors. Mortality of the Wolbachia-free ERK(À) flies may be linked to damage of the epithelial cells triggered by DCV oral infection.…”

Section: Discussionmentioning

confidence: 99%

Impact of ERK activation on fly survival and Wolbachia-mediated protection during virus infection

Wong

Brownlie

Johnson

2016

Journal of General Virology

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Elevated levels of reactive oxygen species (ROS) provide protection against virus-induced mortality in Drosophila. In addition to contributing to oxidative stress, ROS are known to activate a number of signalling pathways including the extracellular signal-regulated kinases (ERK) signalling cascade. It was recently shown that ERK signalling is important for resistance against viral replication and invasion in cultured Drosophila cells and the gut epithelium of adult flies. Here, using a Drosophila loss-of-function ERK (rolled) mutant we demonstrated that ERK is important for fly survival during virus infection. ERK mutant flies subjected to Drosophila C virus (DCV) oral and systemic infection were more susceptible to virus-induced mortality as compared with wild-type flies. We have demonstrated experimentally that ERK activation is important for fly survival during oral and systemic virus infection. Given that elevated ROS correlates with Wolbachia-mediated antiviral protection, we also investigated the involvement of ERK in antiviral protection in flies infected by Wolbachia. The results indicate that ERK activation is increased in the presence of Wolbachia but this does not appear to influence Wolbachia-mediated antiviral protection, at least during systemic infection.

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Section: Discussionmentioning

confidence: 99%

Impact of ERK activation on fly survival and Wolbachia-mediated protection during virus infection

Wong

Brownlie

Johnson

2016

Journal of General Virology

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“…DCV is a single‐stranded positive‐sense RNA virus in the family Dicistroviridae (Christian 1987; Arnold et al . 2013). The sigma virus is a single‐stranded negative‐sense RNA virus in the rhabdovirus family that is a specialist on D. melanogaster (Brun & Plus 1980; Longdon et al .…”

Section: Introductionmentioning

confidence: 99%

“…DCV is a very virulent virus, with infection causing a depression of the metabolic rate followed by death (Arnold et al . 2013). By contrast, the sigma virus does not kill flies, but it is thought to cause a approximately 20% reduction in their fitness (Yampolsky et al .…”

Section: Introductionmentioning

confidence: 99%

The genetic architecture of resistance to virus infection in Drosophila

et al. 2016

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Variation in susceptibility to infection has a substantial genetic component in natural populations, and it has been argued that selection by pathogens may result in it having a simpler genetic architecture than many other quantitative traits. This is important as models of host–pathogen co‐evolution typically assume resistance is controlled by a small number of genes. Using the Drosophila melanogaster multiparent advanced intercross, we investigated the genetic architecture of resistance to two naturally occurring viruses, the sigma virus and DCV (Drosophila C virus). We found extensive genetic variation in resistance to both viruses. For DCV resistance, this variation is largely caused by two major‐effect loci. Sigma virus resistance involves more genes – we mapped five loci, and together these explained less than half the genetic variance. Nonetheless, several of these had a large effect on resistance. Models of co‐evolution typically assume strong epistatic interactions between polymorphisms controlling resistance, but we were only able to detect one locus that altered the effect of the main effect loci we had mapped. Most of the loci we mapped were probably at an intermediate frequency in natural populations. Overall, our results are consistent with major‐effect genes commonly affecting susceptibility to infectious diseases, with DCV resistance being a near‐Mendelian trait.

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“…However, virus-induced pathologies in flies still are poorly understood (21,22). Here, we have investigated an aspect of the pathology caused by DCV, a natural pathogen of Drosophila frequently used to investigate antiviral immunity.…”

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confidence: 99%

Drosophila C Virus Systemic Infection Leads to Intestinal Obstruction

Chtarbanova

Lamiable

Lee

et al. 2014

J Virol

104

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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. IMPORTANCEDCV 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.

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Physiological and metabolic consequences of viral infection in Drosophila melanogaster

Cited by 78 publications

References 60 publications

Impact of ERK activation on fly survival and Wolbachia-mediated protection during virus infection

Impact of ERK activation on fly survival and Wolbachia-mediated protection during virus infection

The genetic architecture of resistance to virus infection in Drosophila

Drosophila C Virus Systemic Infection Leads to Intestinal Obstruction

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