Pre-existing malaria prevents secondary infection by another Plasmodium strain, the parasite responsible for malaria, by restricting iron availability in the liver of the host. These findings, published online this week in Nature Medicine, may have implications for iron supplementation used to combat anaemia in malaria-endemic regions.
Superinfection by multiple Plasmodium species is not common in very young children in spite of their low level of immunity to the parasite. To understand why, Maria Mota and colleagues modelled Plasmodium superinfection in mice.
They show that above a threshold level of parasites in the blood, the blood stage infection held in check the liver stage development of superinfected parasites by stimulating up-regulation of the host’s hepcidin ― the iron regulatory hormone. Increased hepcidin reduced the availability of iron in liver cells, where it is essential for successful development of liver stage parasites. In contrast, iron supplementation increased liver stage development of the superinfected Plasmodium species.