Despite much work in basic and applied research, malaria remains, 120 years after the identification of Plasmodium, a major health issue, particularly in Africa
[1–3]. Vector control is an important component of malaria control, and insecticide-treated nets (ITNs) and indoor residual spraying (IRS) are the front-line tools
[4, 5]. Currently, pyrethroids are the only class of insecticides approved for treating bed nets because of their effectiveness, with a strong excito-repellent effect on mosquitoes, and their lower mammalian toxicity than organochlorine, carbamate and organophosphate compounds
. Unfortunately, a gene-conferring resistance (knock-down resistance, kdr) to pyrethroids and cross-resistance to DDT, first reported in Anopheles gambiae s.s. populations in Côte d’Ivoire
, has spread, mainly in West Africa. kdr, resulting from a single point mutation was probably due first to intensive use of DDT and then pyrethroids for crop protection, particularly in cotton-growing areas and at lower rates for domestic protection
. The efficacy of ITNs for preventing malaria is well established and they are known to provide substantial protection to both individuals and communities using them
. Several studies have shown a direct relationship between the rapid increase in the frequency of kdr and widespread use of bed nets, with a rebound of malaria as a direct consequence
In West Africa, the principal malaria vectors are members of the An. gambiae complex
. Over the past 15 years, several research teams have agreed on a molecular approach to speciate An. gambiae s.s. Five sympatric and syntopic chromosomal forms of An. gambiae s.s. have been described and designated with non-Linnean nomenclature as bamako, bissau, forest, mopti and savanna
[13–15]. The pattern of molecular markers revealed the existence of two genetic variants, referred to as molecular M and S forms
[16–18]. No association was found between speciation and chromosomal constitution, which seems to be involved in ecotypic adaptation. Although chromosome inversions and even chromosome-2 karyotypes are shared between molecular forms, there is a significant lack of gene flow between the M and S forms because of the absence or rarity of hybrid rDNA genotypes
[14, 19, 20], as seen in geographically comprehensive surveys in Africa
[17, 18, 21–23]. Whatever the geographical region, however, gene flow between the M and S forms is very limited, resulting in the current speciation. On the basis of the investigation of Reidenbach et al.
 on the genomes of paired population samples of M and S from Burkina Faso, Cameroon and Mali, Coetzee et al.
 assigned the name An. gambiae to the S molecular form and Anopheles coluzzii to the M form.
Plasmodium species, the agents of malaria, are exclusively transmitted by Anopheles mosquitoes. The susceptibility of these mosquitoes to Plasmodium infection is related to their ability to allow parasite development from gamete fertilization through to sporozoite production. During sporogonic development in the mosquito midgut lumen, midgut epithelium and haemolymph, the parasites face a hostile environment, leading to a considerable reduction in the number that reach the oocyst stage
[26–28]. Mosquito susceptibility is the result of evolutionary processes in both the parasite and the vector, which maintain susceptible and refractory alleles in natural populations. Susceptibility is highly variable, ranging from total refractoriness to high receptiveness depending on both parasite and vector status and their interactions
. In the context of generalization of insecticide resistance, the hypothesis that insecticide resistance has a positive impact on the capacity of mosquitoes to transmit malaria constitutes a hindrance for malaria elimination
The aim of this study was to test whether the kdr mutation in wild An. gambiae affects its susceptibility to Plasmodium infection. As populations of An. coluzzii (previously molecular form M) and An. gambiae S molecular form have been shown to have different susceptibilities to Plasmodium
. These studies investigated these two populations to assess whether the genotype at the kdr locus is responsible for different susceptibility to Plasmodium falciparum infection.