Research Focus:
How to starve a malaria parasite: unravelling nutrient transport mechanisms in Plasmodium falciparum
Malaria remains one of the most devastating infectious diseases worldwide, affecting hundreds of millions of people each year. Despite recent advances in vaccination and vector control, the spread of resistance to existing antimalarial drugs threatens current treatment strategies and highlights the urgent need for therapies with new mechanisms of action. To address this need, our research aims to elucidate how the malaria parasite Plasmodium falciparum acquires essential nutrients from its human host and to exploit these processes as targets for new antimalarial therapies. By focusing on parasite vulnerabilities that are mechanistically distinct from existing treatments, we seek to open new avenues for combating drug-resistant malaria.
As an obligate intracellular parasite, Plasmodium replicates within host cells and depends on host-derived nutrients to survive (see Figure). During the blood stage of infection, the parasite obtains most of its amino acids through uptake and digestion of haemoglobin from host erythrocytes, producing haemozoin crystals as a by-product of haem detoxification. However, to sustain growth and replication, additional nutrients are required from human serum, including sugars, amino acids, nucleotides, lipids, and vitamins. For their import, the parasite relies on specialised membrane transport proteins. Despite their importance for parasite survival, most Plasmodium membrane transporters remain unidentified or poorly characterised, making them an underexplored class of therapeutic targets with significant untapped potential.
