@article{fdi:010037726,
  title = {{A}nopheles and {P}lasmodium: from laboratory models to natural systems in the field},
  author = {{C}ohuet, {A}nna and {O}sta, {M}. {A}. and {M}orlais, {I}sabelle and {A}wono {A}mbene, {P}. {H}. and {M}ichel, {K}. and {S}imard, {F}r{\'e}d{\'e}ric and {C}hristophides, {G}. {K}. and {F}ontenille, {D}idier and {K}afatos, {F}. {C}.},
  editor = {},
  language = {{ENG}},
  abstract = {{P}arasites that cause malaria must complete a complex life cycle in {A}nopheles vector mosquitoes in order to be transmitted from human to human. {P}revious gene-silencing studies have shown the influence of mosquito immunity in controlling the development of {P}lasmodium. {T}hus, parasite survival to the oocyst stage increased when the parasite antagonist gene {LRIM}1 (leucine-rich repeat immune protein 1) of the mosquito was silenced, but decreased when the {C}-type lectin agonist gene {CTL}4 or {CTLMA}2 ({CTL} mannose binding 2) was silenced. {H}owever, such effects were shown for infections of the human mosquito vector {A}nopheles gambiae with the rodent parasite {P}lasmodium berghei. {H}ere, we report the first results of {A}. gambiae gene silencing on infection by sympatric field isolates of the principal human pathogen {P}. falciparum. {I}n contrast with the results obtained with the rodent parasite, silencing of the same three genes had no effect on human parasite development. {T}hese results highlight the importance of following up discoveries in laboratory model systems with studies on natural parasite-mosquito interactions.},
  keywords = {{A}nopheles ; immunity ; model ; natural conditions ; {P}lasmodium},
  booktitle = {},
  journal = {{EMBO} {R}eports},
  volume = {7},
  numero = {12},
  pages = {1285--1289},
  ISSN = {1469-221{X}},
  year = {2006},
  DOI = {10.1038/sj.embor.7400831},
  URL = {https://www.documentation.ird.fr/hor/fdi:010037726},
}