Plasmodium parasite exploits host aquaporin-3 during liver stage malaria infection

Abstract

Author summary Plasmodium parasites undergo an obligatory morphogenesis and replication within the liver before they invade red blood cells and cause malaria. The liver stage is clinically silent but essential for the Plasmodium parasite to complete its life cycle. During this time, the parasite relies on the host cell to support a massive replication event, yet host factors that are critical to this expansion are largely unknown. We identify human aquaporin-3 (AQP3), a water and glycerol channel, as essential for the proper development of the parasite within the liver cell. AQP3 localizes to the parasitophorous vacuole membrane, the interface between the host cytoplasm and the parasite, possibly aiding in the nutritional uptake for the parasite. Genetic disruption or treatment with the AQP3 inhibitor auphen, reduces parasite load in liver and blood cells.