MAHRP2 is required for tether formation and cytoadherence in Plasmodium falciparum infected red blood cells

Abstract

The ability of the human malaria parasite Plasmodium falciparum to remodel its host red blood cell (RBC) is central to the parasite’s ability to survive within the circulation of its host and cause disease. Following invasion, the parasite exports proteins into the RBC cytoplasm where they remodel the membrane skeleton and alter the cell’s biophysical properties. Many of the exported proteins are trafficked through parasite derived structures called Maurer’s clefts in the cytoplasm of the RBC. These clefts act as an intermediate compartment for proteins en route to the RBC membrane such as the major virulence protein, Plasmodium falciparum Erythrocyte Membrane Protein 1 (PfEMP1). From the Ma..