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Anopheles gambiae  s.s. mosquitoes are efficient vectors for  Plasmodium falciparum , although variation exists in their susceptibility to infection. This variation depends partly on the thioester-containing protein 1 (TEP1) and TEP depletion results in significantly elevated numbers of oocysts in susceptible and resistant mosquitoes. Polymorphism in the  Plasmodium  gene coding for the surface protein Pfs47 modulates resistance of some parasite laboratory strains to TEP1-mediated killing. Here, we examined resistance of  P. falciparum  isolates of African origin (NF54, NF165 and NF166) to TEP1-mediated killing in a susceptible Ngousso and a refractory L3–5 strain of  A. gambiae . All parasite clones successfully developed in susceptible mosquitoes with limited evidence for an impact of TEP1 on transmission efficiency. In contrast, NF166 and NF165 oocyst densities were strongly reduced in refractory mosquitoes and  TEP1  silencing significantly increased oocyst densities. Our results reveal differences between African  P. falciparum  strains in their capacity to evade TEP1-mediated killing in resistant mosquitoes. There was no significant correlation between  Pfs47  genotype and resistance of a given  P. falciparum  isolate for TEP1 killing. These data suggest that polymorphisms in this locus are not the sole mediators of immune evasion of African malaria parasites.

Variation in susceptibility of African Plasmodium falciparum malaria parasites to TEP1 mediated killing in Anopheles gambiae mosquitoes