(A) P. falciparum Mrz (B–G) parasite ligands and RBC receptors involved in initial contact, apical reorientation and tight junction formation during Mrz invasion of RBC. (H) P. falciparum ring stage growing inside the PVM, representing the interface between parasite and host cytoplasm. Maurer’s clefts are flat and elongated membrane vesicles; they are mobile in iRBC cytoplasm during early parasite stages. (I) P. falciparum trophozoite stage. Maurer’s clefts are attached to membrane skeleton during mature parasite stages. Tubovesicular network (TVN) extending from the PVM into iRBC cytoplasm. Caveola vesicle complex (CVC) containing P. falciparum antigens which could be involved in the transport and release of specific parasite antigens from the iRBC and in plasma protein uptake. J dots, K dots and exosomes are membrane structures that traffic some parasite proteins (e.g. PfEMP-1) through iRBC cytoplasm. Knobs covering the iRBC surface during late parasite stages. (J) P. falciparum cytoadherence mediated by the interaction between variant surface antigens and host receptors (K) P. falciparum schizont stage. (K) iRBC rupture and Mrz release. (L) Mrz release and RBC reinvasion. Molina-Franky J, Patarroyo ME, Kalkum M, Patarroyo MA. The Cellular and Molecular Interaction Between Erythrocytes and Plasmodium falciparum Merozoites. Front Cell Infect Microbiol. 2022 12:816574. PMID: 35433504