Role of exported proteins in the intracellular dynamics of liver-stage falciparum malaria

Malaria is one of the most important parasitic infections of humans. Every year more than 250 million people contract malaria resulting in 1 million deaths, mostly African children, and Plasmodium falciparum is responsible for the most severe disease.
The key to successful infection in humans is the parasite’s ability to evade the immune system by living within host cells. First, the parasite invades hepatocytes and approximately one week later emerges to infect erythrocytes. The liver-stage of malaria is clinically silent; however, when erythrocytes are infected, the parasite exports several hundred proteins beyond the vacuole membrane to remodel the cell. Erythrocyte remodeling is responsible for the devastating manifestations of falciparum malaria. During the liver-stage parasites grow in hepatocytes within a vacuole without eliciting an immune response. Intracellular development involves blocking host cell apoptosis; however, genetically modified parasites are often killed in a T cell-dependent manner that provides protective immunity. Thus, studies focused on the liver-stage of malaria have profound significance and may guide the development of new antimalarials or a vaccine. 

Basic Science

May 2012 — Apr 2015

Australia