@article{fdi:010078586,
  title = {{I}nfection intensity-dependent responses of {A}nopheles gambiae to the {A}frican malaria parasite {P}lasmodium falciparum},
  author = {{M}endes, {A}. {M}. and {A}wono-{A}mbene, {P}. {H}. and {N}sango, {S}. {E}. and {C}ohuet, {A}nna and {F}ontenille, {D}idier and {K}afatos, {F}. {C}. and {C}hristophides, {G}. {K}. and {M}orlais, {I}sabelle and {V}lachou, {D}.},
  editor = {},
  language = {{ENG}},
  abstract = {{M}alaria remains a devastating disease despite efforts at control and prevention. {E}xtensive studies using mostly rodent infection models reveal that successful {P}lasmodium parasite transmission by the {A}frican mosquito vector {A}nopheles gambiae depends on finely tuned vector-parasite interactions. {H}ere we investigate the transcriptional response of {A}. gambiae to geographically related {P}lasmodium falciparum populations at various infection intensities and different infection stages. {T}hese responses are compared with those of mosquitoes infected with the rodent parasite {P}lasmodium berghei. {W}e demonstrate that mosquito responses are largely dependent on the intensity of infection. {A} major transcriptional suppression of genes involved in the regulation of midgut homeostasis is detected in low-intensity {P}. falciparum infections, the most common type of infection in {A}frica. {I}mportantly, genes transcriptionally induced during these infections tend to be phylogenetically unique to {A}. gambiae. {T}hese data suggest that coadaptation between vectors and parasites may act to minimize the impact of infection on mosquito fitness by selectively suppressing specific functional classes of genes. {RNA} interference ({RNA}i)-mediated gene silencing provides initial evidence for important roles of the mosquito {G} protein-coupled receptors ({GPCR}s) in controlling infection intensity-dependent antiparasitic responses.},
  keywords = {},
  booktitle = {},
  journal = {{I}nfection and {I}mmunity},
  volume = {79},
  numero = {11},
  pages = {4708--4715},
  ISSN = {0019-9567},
  year = {2011},
  DOI = {10.1128/iai.05647-11},
  URL = {https://www.documentation.ird.fr/hor/fdi:010078586},
}