Malaria

Malaria causes over 200 million clinical cases and more than half a million deaths each year, the majority among children below 5 years old in Sub-Saharan Africa. The symptoms and pathology of malaria arise exclusively during the blood stage of infection, when Plasmodium parasites invade and replicate within red blood cells.

Plasmodium is a unicellular parasite that infects a broad range of hosts, including reptiles, birds, and mammals. Five species infect humans via the bite of an infected female Anopheles mosquito. Among them, Plasmodium falciparum is the most lethal and the primary focus of our research. P. falciparum completes a 48-hour developmental cycle inside red blood cells and uniquely causes infected cells to adhere to the microvasculature—a process known as sequestration. The invasion of red blood cells is a rapid and highly specific event, typically completed in under a minute and involving multiple receptor–ligand interactions. This step is essential for parasite replication and marks a brief moment when the parasite is exposed to antibody-mediated immune responses, making it a prime target for vaccines and drugs. Sequestration, meanwhile, allows parasites to evade clearance by the spleen and leads to the accumulation of infected cells in small vessels, resulting in obstruction, inflammation, hypoxia, and localised haemorrhage—key contributors to disease severity and organ-specific complications such as brain swelling in cerebral malaria.