Mendes A. M., Awono-Ambene P. H., Nsango S. E., Cohuet Anna, Fontenille Didier, Kafatos F. C., Christophides G. K., Morlais Isabelle, Vlachou D. (2011). Infection intensity-dependent responses of Anopheles gambiae to the African malaria parasite Plasmodium falciparum. Infection and Immunity, 79 (11), p. 4708-4715. ISSN 0019-9567.
Titre du document
Infection intensity-dependent responses of Anopheles gambiae to the African malaria parasite Plasmodium falciparum
Mendes A. M., Awono-Ambene P. H., Nsango S. E., Cohuet Anna, Fontenille Didier, Kafatos F. C., Christophides G. K., Morlais Isabelle, Vlachou D.
Source
Infection and Immunity, 2011,
79 (11), p. 4708-4715 ISSN 0019-9567
Malaria remains a devastating disease despite efforts at control and prevention. Extensive studies using mostly rodent infection models reveal that successful Plasmodium parasite transmission by the African mosquito vector Anopheles gambiae depends on finely tuned vector-parasite interactions. Here we investigate the transcriptional response of A. gambiae to geographically related Plasmodium falciparum populations at various infection intensities and different infection stages. These responses are compared with those of mosquitoes infected with the rodent parasite Plasmodium berghei. We 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 Africa. Importantly, genes transcriptionally induced during these infections tend to be phylogenetically unique to A. gambiae. These 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 (RNAi)-mediated gene silencing provides initial evidence for important roles of the mosquito G protein-coupled receptors (GPCRs) in controlling infection intensity-dependent antiparasitic responses.
