Makhtar Niang

TL;DR: A rise in resistance to artemisinin derivatives in field isolates indicates the need for increased vigilance and a coordinated and rapid deployment of drug combinations.

TL;DR: STEVOR functions as an erythrocyte-binding protein that recognizes Glycophorin C on the red blood cell (RBC) surface and that its binding correlates with the level of GPC on the RBC surface, suggesting a PfEMP1-independent role for STEVOR in enabling infected ERYthrocytes at the schizont stage to form rosettes and in promoting merozoite invasion.

TL;DR: It is shown that mature GIEs are more deformable than immature stages using ektacytometry and microsphiltration methods, and that a switch in cellular deformability in the transition from immature to mature gametocytes is accompanied by the deassociation of parasite-derived STEVOR proteins from the infected erythrocyte membrane.

TL;DR: It is demonstrated that to obtain a complete understanding of how parasite-induced pathology is linked to variation on the surface of the iRBC, focusing the interactions of multiple multigene families needs to be considered.

TL;DR: Genetic drift alone cannot explain the observed polymorphism, suggesting that other evolutionary mechanisms are operating and one possible contributor could be the frequency of haemoglobinopathies that are associated with calcium dysregulation in the erythrocyte.