Premium
Anopheles and Plasmodium : from laboratory models to natural systems in the field
Author(s) -
Cohuet Anna,
Osta Mike A,
Morlais Isabelle,
AwonoAmbene Parfait H,
Michel Kristin,
Simard Frederic,
Christophides George K,
Fontenille Didier,
Kafatos Fotis C
Publication year - 2006
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400831
Subject(s) - biology , anopheles gambiae , parasite hosting , plasmodium berghei , anopheles , malaria , plasmodium (life cycle) , vector (molecular biology) , virology , plasmodium falciparum , gene silencing , rna interference , gene , genetics , immunology , rna , world wide web , computer science , recombinant dna
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.