Plasmodium P47 : a key gene for malaria transmission by mosquito vectors

Abstract

Malaria is caused by infection with Plasmodium parasites that have a complex life cycle. The parasite protein P47 is critical for disease transmission. P47 mediates mosquito immune evasion in both Plasmodium berghei (Pbs47) and Plasmodium falciparum (Pfs47), and has been shown to be important for optimal female gamete fertility in P. berghei. Pfs47 presents strong geographic structure in natural P. falciparum populations, consistent with natural selection of Pfs47 haplotypes by the mosquito immune system as the parasite adapted to new vector species worldwide. These key functions make Plasmodium P47 an attractive target to disrupt malaria transmission.

Plasmodium PIMMS43 is required for ookinete evasion of the mosquito complement-like response and sporogonic development in the oocyst

“…Furthermore, a small-scale genotypic analysis of oocysts sampled from A. gambiae and A. funestus mosquitoes in Tanzania revealed significant differentiation in Pfs47 haplotypes sampled from the two vectors [34]. These data are consistent with natural selection of Pfs47 haplotypes by the mosquito immune system and a key role of this interaction in parasite-mosquito coevolution [32]. However, a different study showed that polymorphisms in the Pfs47 locus alone could not fully explain the observed variation in complement-mediated immune evasion of African P. falciparum strains [35].…”

Sexual forms obtained in a continuous in vitro cultured Colombian strain of Plasmodium falciparum (FCB2)

“…A mosquito's parasite infectivity is related to the parasite's genetic factors enabling mosquitoes to avoid host innate immune response resulting from coevolution of both organisms [15]. Nevertheless, variation in mosquito infectivity has been reported when using P. falciparum isolates from the same geographical area, e.g.…”

“…African strain NF54 infected 90% of Anopheles gambiae, Kenyan strain K39 infected 86% of An. gambiae, whilst M24 infected only 6% of the same mosquito species [15,66]. Plasmodium falciparum FCB2 oocyst production.…”

“…Mosquito immune pressure generates genetic changes in P. falciparum, thereby enabling its gradual adaptation to mosquitoes from different geographical regions [11]. Parasite-vector interaction has been extensively followed up in African mosquitoes because of the ease of parasite isolate availability and the ease of establishing mosquito colonies to facilitate studying the mosquito's immune response [14][15][16][17]. Comparative analysis of parasite compatibility with mosquitoes from Africa and Southeast Asia has found parasite adaptive mechanisms regarding each Anopheles species; a similar approach has been followed with the Latin-American P. falciparum strain 7G8 and Anopheles albimanus [15].…”

“…Parasite-vector interaction has been extensively followed up in African mosquitoes because of the ease of parasite isolate availability and the ease of establishing mosquito colonies to facilitate studying the mosquito's immune response [14][15][16][17]. Comparative analysis of parasite compatibility with mosquitoes from Africa and Southeast Asia has found parasite adaptive mechanisms regarding each Anopheles species; a similar approach has been followed with the Latin-American P. falciparum strain 7G8 and Anopheles albimanus [15]. Even so, knowledge is still lacking about the interaction of other Latin-American parasite strains with New World mosquitoes [18].…”