Journal
NATURE COMMUNICATIONS
Volume 8, Issue -, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41467-017-00610-8
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Funding
- Wellcome Trust [WT095121MA, WT202888/Z/16/Z]
- MRC [MC_PC_15087]
- EU-FP7 award 'InfraVec'
- Wellcome Trust [202888/Z/16/Z] Funding Source: Wellcome Trust
- EPSRC [EP/M028127/1] Funding Source: UKRI
- MRC [MC_PC_15087, MC_UU_12014/8] Funding Source: UKRI
- Engineering and Physical Sciences Research Council [EP/M028127/1] Funding Source: researchfish
- Medical Research Council [MC_PC_15087] Funding Source: researchfish
- Wellcome Trust [202888/Z/16/Z] Funding Source: researchfish
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Wolbachia are intracellular maternally inherited bacteria that can spread through insect populations and block virus transmission by mosquitoes, providing an important approach to dengue control. To better understand the mechanisms of virus inhibition, we here perform proteomic quantification of the effects of Wolbachia in Aedes aegypti mosquito cells and midgut. Perturbations are observed in vesicular trafficking, lipid metabolism and in the endoplasmic reticulum that could impact viral entry and replication. Wolbachia-infected cells display a differential cholesterol profile, including elevated levels of esterified cholesterol, that is consistent with perturbed intracellular cholesterol trafficking. Cyclodextrins have been shown to reverse lipid accumulation defects in cells with disrupted cholesterol homeostasis. Treatment of Wolbachia-infected Ae. aegypti cells with 2-hydroxypropyl-beta-cyclodextrin restores dengue replication in Wolbachia-carrying cells, suggesting dengue is inhibited in Wolbachia-infected cells by localised cholesterol accumulation. These results demonstrate parallels between the cellular Wolbachia viral inhibition phenotype and lipid storage genetic disorders.
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