Plasmodium falciparum parasites deploy RhopH2 into the host erythrocyte to obtain nutrients, grow and replicate

摘要: Plasmodium falciparum parasites, the causative agents of malaria, modify their host erythrocyte to render them permeable supplementary nutrient uptake from plasma and for removal toxic waste. Here we investigate contribution rhoptry protein RhopH2, in formation new permeability pathways (NPPs) Plasmodium-infected erythrocytes. We show RhopH2 interacts with RhopH1, RhopH3, cytoskeleton exported proteins involved cell remodeling. Knockdown expression cycle one leads a depletion essential vitamins cofactors decreased de novo synthesis pyrimidines two. There is also significant impact on parasite growth, replication transition into three. The solutes that use NPPs enter erythrocytes reduced upon knockdown. These findings provide direct genetic support RhopH complex NPP activity highlight importance survival.