Erythrocyte host modifications in Plasmodium falciparum

Malaria is a deadly disease, caused by parasite Plasmodium falciparum, that affects a large percentage of the world’s population. Symptoms of severe malaria arise from the asexual stage of the parasite life cycle, which occurs in human red blood cells. The parasite exports a large number of proteins to the host membrane where the proteins interact with the cytoskeletal network or express on the surface where it binds to human endothelial receptors. This leads to decreased deformability and sequestration of infected cells in microvasculature often leading to organ failure and death. This project worked on characterising the function of a novel export protein, PFB0115w, thought to be involved in the presentation of virulent surface antigens at the host membrane and on developing a flow-based method to quantify deformability of infected cells.