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EMBO reports 7, 12, 1285–1289 (2006)
doi:10.1038/sj.embor.7400831
AOP Published online: 10 November 2006
Anopheles and Plasmodium: from laboratory models to natural systems in the field
Anna Cohuet1, Mike A Osta2, Isabelle Morlais3, Parfait H Awono-Ambene3, Kristin Michel2, Frederic Simard3, George K Christophides2, Didier Fontenille1 & Fotis C Kafatos2
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1 Institut de Recherche pour le Développement—Laboratoire de Lutte contre les Insectes Nuisibles, UR 016, BP 64501, 911 Avenue Agropolis, 34394 Montpellier cedex 5, France
2 Division of Cell and Molecular Biology, Imperial College London, Sir Alexander Fleming Building, South Kensington Campus, London SW7 2AZ, UK
3 Organisation de Coordination de la lutte contre les Endémies en Afrique Centrale, Laboratoire de Recherche sur le Paludisme, Yaounde BP 288, Cameroon
To whom correspondence should be addressed
Anna Cohuet Tel: +33 4 67 41 61 55; Fax: +33 67 54 20 44; E-mail: cohuet@mpl.ird.fr
Fotis C Kafatos Tel: +44 20 7594 1267; Fax: +44 20 7594 2056; E-mail: f.kafatos@imperial.ac.uk
Received 13 April 2006; Accepted 4 September 2006; Published online 10 November 2006.
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Abstract
Parasites that cause malaria must complete a complex life cycle in Anopheles vector mosquitoes in order to be transmitted from human to human. Previous gene-silencing studies have shown the influence of mosquito immunity in controlling the development of Plasmodium. Thus, parasite survival to the oocyst stage increased when the parasite antagonist gene LRIM1 (leucine-rich repeat immune protein 1) of the mosquito was silenced, but decreased when the C-type lectin agonist gene CTL4 or CTLMA2 (CTL mannose binding 2) was silenced. However, such effects were shown for infections of the human mosquito vector Anopheles gambiae with the rodent parasite Plasmodium berghei. Here, we report the first results of A. gambiae gene silencing on infection by sympatric field isolates of the principal human pathogen P. falciparum. In contrast with the results obtained with the rodent parasite, silencing of the same three genes had no effect on human parasite development. These results highlight the importance of following up discoveries in laboratory model systems with studies on natural parasite–mosquito interactions.
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