Interactions between Plasmodium falciparum–infected red blood cells and their extracellular vesicles with megakaryocytes: implications for platelet-like particle formation

Intact pRBCs strongly inhibit megakaryocytic differentiation and disrupt PLP function through transcriptional dysregulation and inflammatory activation, whereas under our experimental conditions, RBC-EVs exert milder modulatory effects. These findings highlight defective platelet production as a novel mechanism contributing to malaria-associated thrombocytopenia.