Human genetics and malaria transmission

Malaria remains the world's deadliest parasitic disease. Its transmission depends on complex interactions among the human host, Anopheles mosquito vectors, and Plasmodium parasites. A key determinant is the density of gametocytes in peripheral blood, which correlates with the burden of the subsequent diploid stage, the ookinete, developing in the mosquito midgut within 24 hours after an infectious blood meal. The human genetic background, shaped by millennia of selective pressure exerted by P. falciparum, plays a central role in these dynamics. Protective genetic variants, such as β-globin mutations (HbS and HbC), thalassemias, and G6PD deficiency, reduce disease severity but may also influence gametocyte production. This project, using innovative molecular tools, will investigate if human genetic polymorphisms affect malaria transmission by correlating host genotypes with mosquito-derived ookinete loads.