Remodelling of the erythrocyte during and after merozoite invasion
Most of the clinical symptoms and the associated mortality and morbidity of falciparum malaria are a result of the parasite undergoing continuous cycles of asexual reproduction within human red blood cells. Infected red blood cells become rigid, poorly deformable, and develop the ability to cytoadhere to a number of cell types such as vascular endothelial cells, a mechanism that prevents the parasitised host cells from passing through to the spleen where they would be cleared from the blood stream. These cellular modifications of the infected red blood cell are the result of a dramatic remodelling process induced by the parasite that ultimately serves to induce cytoadherence by exposing various ligands on the erythrocyte surface for host cell receptors and facilitate nutrient import into the infecting parasite.
Our work is aimed at understanding the role of proteins in this remodelling process and cytoadherence of the infected erythrocyte as this is pivotal to the successful infection of the erythrocyte by this parasite and pathogenesis of the disease. See below for some of our recent publications in this area.
Two parasitised red blood cells
Left - normal; Right - KAHRP KO
