Purpose of review: Plasmodium falciparum causes the most virulent form of human malarias. It is a protozoan parasite that infects human erythrocytes and the erythrocytic stages are responsible for all symptoms and pathologies of the disease. Critical to infection is the formation of a parasitophorous vacuolar membrane at the time of entry and within which the intracellular parasite proliferates. Since erythrocytes lack endocytic machinery, it is surprising that they can be infected by pathogens. This review summarizes recent studies of the erythrocyte-malaria interaction that have provided insights into properties of erythrocyte membranes as well as parasite mechanisms that remodel the erythrocyte.
Recent findings: Themes revealed by recent literature suggest that both parasite and erythrocyte components regulate parasite entry and intracellular growth by extensively remodeling host membranes. These remodeling events include the invagination of the host cell membrane during parasite entry that results in the creation and maintenance of a vacuole that surrounds the intracellular organism, and the development of antigenic, structural and transport alterations during intracellular parasite development.
Summary: The implications are that malarial erythrocyte remodeling events occur at a significant cost to the human host since many of the associated virulence events have been linked to severe disease pathologies.