This parasitic disease is a global scourge that still causes around 600,000 deaths a year, most of them in sub-Saharan Africa, despite major advances in protection and treatment. Plasmodium, the agent of malaria, is a single-celled, intracellular parasite. There are several varieties. The Plasmodium cycle is complex, from inoculation by the mosquito vector to transformation of the parasite in the liver and subsequent multiplication in the blood. Its molecular mechanisms are now better understood. The same applies to the pathophysiology of malaria. The adhesion of infected red blood cells to the vascular endothelium causes significant tissue damage, both directly (obstruction) and indirectly (inflammation). The innate immune response is multifactorial, and a source of pro-inflammatory cytokines that contribute to the pathology. The diversity of adaptive T and B responses (antigenic recognition repertoire and intensity) correlates with better infection control.
Genetic variants in the insect vector, Plasmodium and host influence the severity of infection. This is particularly true of red blood cell (RBC) proteins, certain variants of which protect against malaria by making RBCs resistant to infection. The parasite has also selected protective factors against the immune response. Against this complex backdrop, the generation of effective vaccines is proving an arduous task. However, significant progress has been made in using - among the many potential molecular targets - more or less attenuated whole forms of the parasite. Several clinical studies are encouraging in this respect.
16:30 - 18:00
