Spread of refractoriness linked to a transposon as a genetic drive mechanism and its effect on the prevalence of malaria in the human population at equilibrium. Panels (a)-(d) show the efficacy of the genetic drive mechanism (i.e. the proportion of heterozygotes that turn homozygous) that is required for refractoriness to spread to fixation. Panels (a) and (c) assume that the cost refractoriness is fixed, panels (b) and (d) assume a conditional cost induced by parasite infection. Panel (e) shows the effect of fixation of the allele coding for refractoriness on the prevalence of malaria. The parameters used to simulate the equations were: biting rate a = 0.5 day-1, mortality μ = 0.1 day-1, virulence = 0.1 and dominance h = 0.9. In panels (a) and (c) the efficacy of refractoriness was held at s = 1, the initial intensity of was set to R0,init = 30 and the cost of refractoriness and the cost of the transposon (i.e. before the spread of refractoriness) were varied. In panels (b) and (d) the cost of refractoriness was held at c = 0.2, the cost of the transposon was held at c
= 0.05, and the efficacy of refractoriness and the initial intensity of transmission were varied. In panel (e) the parameters not mentioned above were chosen to allow fixation of refractoriness.