Mechanisms of infected erythrocyte adhesion to endothelium in cerebral malaria. Early in the blood stage of P falciparum infection, endothelial cells become activated to secrete ULVWF strands, which remain attached to the endothelial surface and rapidly bind platelets. Infected erythrocytes, coated with membrane knobs rich in PfEMP1, adhere to the platelet-decorated ULVWF strings through platelet CD36. ULVWF contributes to both the thrombocytopenia and hemolytic anemia of malaria by binding large numbers of platelets and by shearing red cells.