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dc.contributor.authorChilds, Lauren M.
dc.contributor.authorCai, Francisco Y.
dc.contributor.authorKakani, Evdoxia G.
dc.contributor.authorMitchell, Sara N.
dc.contributor.authorPaton, Doug
dc.contributor.authorGabrieli, Paolo
dc.contributor.authorBuckee, Caroline O.
dc.contributor.authorCatteruccia, Flaminia
dc.date.accessioned2018-12-04T18:42:14Z
dc.date.available2018-12-04T18:42:14Z
dc.date.issued2016-12-15
dc.identifier.issn1553-7366
dc.identifier.othere1006060
dc.identifier.urihttp://hdl.handle.net/10919/86216
dc.description.abstractThe control of mosquito populations with insecticide treated bed nets and indoor residual sprays remains the cornerstone of malaria reduction and elimination programs. In light of widespread insecticide resistance in mosquitoes, however, alternative strategies for reducing transmission by the mosquito vector are urgently needed, including the identification of safe compounds that affect vectorial capacity via mechanisms that differ from fast-acting insecticides. Here, we show that compounds targeting steroid hormone signaling disrupt multiple biological processes that are key to the ability of mosquitoes to transmit malaria. When an agonist of the steroid hormone 20-hydroxyecdysone (20E) is applied to Anopheles gambiae females, which are the dominant malaria mosquito vector in Sub Saharan Africa, it substantially shortens lifespan, prevents insemination and egg production, and significantly blocks Plasmodium falciparum development, three components that are crucial to malaria transmission. Modeling the impact of these effects on Anopheles population dynamics and Plasmodium transmission predicts that disrupting steroid hormone signaling using 20E agonists would affect malaria transmission to a similar extent as insecticides. Manipulating 20E pathways therefore provides a powerful new approach to tackle malaria transmission by the mosquito vector, particularly in areas affected by the spread of insecticide resistance.en_US
dc.description.sponsorshipCOB, FYC and LMC were supported by Award Number U54GM088558 from the National Institute Of General Medical Sciences (NIGMS). The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIGMS or the NIH. FC and SNM were partially supported by a NIH grant (grant ID: NIH 1R01A1104956-01A1), while FC, EGK, PG and DP were partially supported by the European Research Council FP7 ERC Starting Grant Anorep (grant ID: 260897) and by Harvard T. H. Chan School of Public Health funds. FC and DP were supported by the Bill & Melinda Gates Foundation (Grant ID: OPP1140143). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
dc.format.extent20 pages
dc.format.mimetypeapplication/pdf
dc.language.isoen_US
dc.publisherPLOS
dc.rightsCreative Commons Attribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectanopheles-gambiaeen_US
dc.subjectculex-quinquefasciatusen_US
dc.subjectplasmodium-falciparumen_US
dc.subjectlepidoptera-noctuidaeen_US
dc.subjectpopulation-dynamicsen_US
dc.subjectecdysone agonistsen_US
dc.subjectjuvenile-hormoneen_US
dc.subjectaquatic stagesen_US
dc.subjectwestern kenyaen_US
dc.subjectinsecticidesen_US
dc.titleDisrupting Mosquito Reproduction and Parasite Development for Malaria Controlen_US
dc.typeArticle - Refereed
dc.title.serialPLOS Pathogens
dc.identifier.doihttps://doi.org/10.1371/journal.ppat.1006060
dc.identifier.volume12
dc.identifier.issue12
dc.type.dcmitypeText
dc.identifier.pmid27977810
dc.identifier.eissn1553-7374


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Creative Commons Attribution 4.0 International
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