Evaluation of resistance to pyrethroid and organophosphate adulticides and kdr genotyping in Aedes aegypti populations from Roraima, the northernmost Brazilian State
PARASITES & VECTORS
Authors: Nogueira Hayd, Ramao Luciano; Carrara, Luana; Lima, Joel de Melo; Vargas de Almeida, Nathalia Coelho; Pereira Lima, Jose Bento; Martins, Ademir
Abstract
BackgroundRoraima, the northernmost State in Brazil, borders Venezuela and Guyana. Although mostly covered by the tropical forests, the urban centers of this state are highly infested with Ae. aegypti and are endemic for dengue, Zika and chikungunya. We accessed the insecticide resistance status of Ae. aegypti populations from the capital Boa Vista, two cities on international borders (Pacaraima and Bonfim) and Rorainopolis bordering Amazonas State, in order to evaluate the chemical control efficacy in these localities.MethodsTests with World Health Organization (WHO)-like tubes impregnated with the pyrethroid deltamethrin (0.05% and 0.12%) and the organophosphate malathion (0.7%) were conducted with Ae. aegypti from Boa Vista, Pacaraima, Bonfim and Rorainopolis, collected in 2016 and 2018. Genotyping of kdr mutations, related to resistance to pyrethroids, was performed for the SNP variations at sites 1016 and 1534 of the voltage gated sodium channel gene (Na-V) with a TaqMan qPCR approach.ResultsAedes albopictus was absent in our collections, and therefore only Ae. aegypti was tested. All Ae. aegypti populations were susceptible to 0.7% malathion in 2016; however, mortality dropped to under 90% in Bonfim and Pacaraima populations in 2018. All populations were resistant to 0.05% deltamethrin in both years. The time that 50% of females suffered knockdown (KdT(50)) under exposure to 0.05% deltamethrin was 3.3-5.9-fold longer in mosquitoes from the natural populations compared to the susceptible Rockefeller strain. Only the Pacaraima population (2018) remained resistant to 0.12% deltamethrin. Kdr genotyping revealed the absence of the wild-type NaVS haplotype (1016Val+1534Phe) in the populations from Roraima, indicating that all tested insects had a genetic background for pyrethroid resistance. The double kdr Na(V)R2 haplotype (1016Ile+15434Cys) was present in higher frequencies in all populations except for Rorainopolis, where this haplotype seems to have arrived recently.ConclusionsThese results are important for the knowledge about insecticide resistance status of Ae. aegypti populations from Roraima and will help improve vector control strategies that may be applied to diverse localities under similar geographical and urban conditions.
Disruption of the pancreatic vasculature in zebrafish affects islet architecture and function
DEVELOPMENT
Authors: Mullapudi, Sri Teja; Boezio, Giulia L. M.; Rossi, Andrea; Marass, Michele; Matsuoka, Ryota L.; Matsuda, Hiroki; Helker, Christian S. M.; Yang, Yu Hsuan Carol; Stainier, Didier Y. R.
Abstract
A dense local vascular network is crucial for pancreatic endocrine cells to sense metabolites and secrete hormones, and understanding the interactions between the vasculature and the islets may allow for therapeutic modulation in disease conditions. Using live imaging in two models of vascular disruption in zebrafish, we identified two distinct roles for the pancreatic vasculature. At larval stages, expression of a dominant negative version of Vegfaa (dnVegfaa) in beta-cells led to vascular and endocrine cell disruption with a minor impairment in beta-cell function. In contrast, expression of a soluble isoform of Vegf receptor 1 (sFlt1) in beta-cells blocked the formation of the pancreatic vasculature and drastically stunted glucose response, although islet architecture was not affected. Notably, these effects of dnVegfaa or sFlt1 were not observed in animals lacking vegfaa, vegfab, kdrl, kdr or flt1 function, indicating that they interfere with multiple ligands and/or receptors. In adults, disrupted islet architecture persisted in dnVegfaa-expressing animals, whereas sFlt1-expressing animals displayed large sheets of beta-cells along their pancreatic ducts, accompanied by impaired glucose tolerance in both models. Thus, our study reveals novel roles for the vasculature in patterning and function of the islet.