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Paton, Douglas

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Paton, Douglas

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Author's Publications: search.filters.isAuthorOfPublication.2fdc32d8-5b81-453e-950b-3ade1aa57e04

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    Exposing Anopheles mosquitoes to antimalarials blocks Plasmodium parasite transmission
    (Springer Nature, 2019-02-27) Paton, Douglas; Itoe, Maurice; Holmdahl, Inga; Buckee, Caroline; Catteruccia, Flaminia
    Every year the bites of Anopheles mosquitoes kill hundreds of thousands of people, mostly young African children, by transmitting deadly Plasmodium falciparum malaria parasites. Since the turn of the century, efforts to prevent transmission of these parasites via the mass distribution of insecticide-treated bed nets have been extremely successful, causing an unprecedented reduction in malaria deaths1. However, resistance to insecticides has become widespread in Anopheles populations2-4, threatening a global resurgence of the disease and making the generation of effective new malaria control tools an urgent public health priority. Here, we show that development of P. falciparum can be rapidly and completely blocked when Anopheles gambiae females uptake low concentrations of specific antimalarials from treated surfaces, simulating contact with a bed net. Mosquito exposure to atovaquone prior to or shortly after P. falciparum infection causes full parasite arrest in the female midgut, preventing transmission of infection. Similar transmission-blocking effects are achieved with other cytochrome B inhibitors, demonstrating that parasite mitochondrial function is a good target for parasite killing. Incorporating these effects into a model of malaria transmission dynamics predicts that the inclusion of Plasmodium inhibitors on mosquito nets would significantly mitigate the global health impact of insecticide resistance. This study identifies a powerful new strategy for blocking Plasmodium transmission by Anopheles females, with promising implications for malaria eradication efforts.
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    Steroid Hormone Function Controls Non-competitive Plasmodium Development in Anopheles
    (Elsevier BV, 2019-04) Werling, Kristine; Shaw, William; Itoe, Maurice; Westervelt, Kathleen; Marcenac, Perrine; Paton, Douglas; Peng, Duo; Singh, Naresh; Smidler, Andrea L.; South, Adam; Deik, Amy; Mancio-Silva, Liliana; Demas, Allison R.; March, Sandra; Calvo, Eric; Bhatia, Sangeeta; Clish, Clary B.; Catteruccia, Flaminia
    Transmission of malaria parasites occurs when a female Anopheles mosquito feeds on an infected host to acquire nutrients for egg development. How parasites are affected by oogenetic processes, principally orchestrated by the steroid hormone 20-hydroxyecdysone (20E), remains largely unknown. Here we show that Plasmodium falciparum development is intimately but not competitively linked to processes shaping Anopheles gambiae reproduction. We unveil a 20E-mediated positive correlation between egg and oocyst numbers, such that impairing oogenesis by multiple 20E manipulations decreases parasite intensities. These manipulations, however, accelerate Plasmodium growth rates, allowing sporozoites to become infectious sooner. Parasites exploit mosquito lipids for faster growth, but they do so without further impacting egg development. These results suggest that P. falciparum has adopted a non-competitive evolutionary strategy of resource exploitation to optimize transmission while minimizing fitness costs to its mosquito vector. Our findings have profound implications for currently proposed control strategies aimed at suppressing mosquito populations.