Florian Dupuy

TL;DR: Pharmacological agents that raise cAMP levels in transmissible stage V gametocytes render them less deformable and hence less likely to circulate through the spleen, and represent new candidate drugs to block transmission of malaria parasites, such as sildenafil.

TL;DR: Evidence is produced that the increase of GIE stiffness induced by sildenafil (Viagra) is dependent on STEVOR phosphorylation status and on another independent mechanism, and new insights are provided into mechanisms by which phosphodiesterase inhibitors may block malaria parasite transmission.

TL;DR: It is shown that chemically immune-modulated NSG mice grafted with human erythrocytes support complete sexual development of P. falciparum parasites and generate high gametocytemia, and provides the missing link between current in vitro assays and Phase I trials in humans for testing new malariagametocytidal drugs.

TL;DR: It is found that infection of erythroblasts by gametocytes and parasite-derived extracellular vesicles delay the erythroid differentiation, thereby allowing gametocyte maturation to coincide with the release of their host cell from the bone marrow and provide further insights on how Plasmodium parasites interfere with erythropoiesis and contribute to anemia in malaria patients.

TL;DR: Investigation of gametocyte-infected erythrocytes infected with P. falciparum asexual stages and clonal lines and transgenic parasites used to determine whether adhesion may be dependent on binding of STEVOR proteins to Glycophorin C on the surface of erythroid cells indicates that GIE overexpressing STevOR do not specifically adhere to ery throatblasts.