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Iron and copper chelation restricts  Plasmodium  growth  in vitro  and in mammalian hosts. The parasite alters metal homeostasis in red blood cells to its favor, for example metabolizing hemoglobin to hemozoin. Metal interactions with the mosquito have not, however, been studied. Here, we describe the metallomes of  Anopheles albimanus  and  Aedes aegypti  throughout their life cycle and following a blood meal. Consistent with previous reports, we found evidence of maternal iron deposition in embryos of  Ae .  aegypti , but less so in  An .  albimanus . Sodium, potassium, iron, and copper are present at higher concentrations during larval developmental stages. Two  An .  albimanus  phenotypes that differ in their susceptibility to  Plasmodium berghei  infection were studied. The susceptible  white stripe  ( ws ) phenotype was named after a dorsal white stripe apparent during larval stages 3, 4, and pupae. During larval stage 3,  ws  larvae accumulate more iron and copper than the resistant  brown stripe  ( bs ) phenotype counterparts. A similar increase in copper and iron accumulation was also observed in the susceptible  ws , but not in the resistant  bs  phenotype following  P .  berghei  infection. Feeding  ws  mosquitoes with extracellular iron and copper chelators before and after receiving  Plasmodium -infected blood protected from infection and simultaneously affected follicular development in the case of iron chelation. Unexpectedly, the application of the iron chelator to the  bs  strain reverted resistance to infection. Besides a drop in iron, iron-chelated  bs  mosquitoes experienced a concomitant loss of copper. Thus, the effect of metal chelation on  P .  berghei  infectivity was strain-specific.

Mosquito metallomics reveal copper and iron as critical factors for Plasmodium infection