P. falciparum infected RBCs Activators

Plasmodium falciparum is a unicellular protozoan parasite that causes malaria in humans. During its complex life cycle, P. falciparum invades red blood cells (RBCs), drastically modifying them to ensure its survival and propagation.Upon invasion, P. falciparum resides in a vacuole within the RBC and begins to remodel the host cell. This includes changing the RBC's membrane properties, making it stick to the walls of blood vessels, a process known as cytoadherence. This impedes the infected RBC from being transported to the spleen, where it would normally be destroyed.

The parasite also creates 'knobs' on the RBC surface, which are protein structures that play a critical role in cytoadherence. The major protein involved in this process is P. falciparum Erythrocyte Membrane Protein 1 (PfEMP1), which is exported to the RBC surface and interacts with various host receptors.Inside the RBC, the parasite degrades hemoglobin to obtain amino acids for protein synthesis and leaves behind a toxic by-product, hemozoin. The buildup of hemozoin and other metabolic changes can lead to the eventual rupture of the RBC, releasing daughter parasites that can invade other RBCs.P. falciparum-infected RBCs are central to the manifestations of malaria. The sequestration of these cells in blood vessels can cause blockages, leading to severe manifestations such as cerebral malaria.