PROCR and alpha thalassemia spectrum: In one mechanism, HbS and α+thalassemia each impairs binding of parasitized red blood cells (pRBCs) to microvascular endothelial cells (MVECs, cytoadherence) and uninfected RBCs (rosetting), two virulence traits mediated by interactions between P. falciparum erythrocyte membrane protein 1 (PfEMP1) ligands on pRBCs and various receptors (CD36, ICAM1, endothelial protein C receptor [EPCR]) on host cells.