Plasmodium falciparum

We have produced the first ever empirical global map of P. falciparum risk using rigorous geo-statistical models of infection prevalence, remotely sensed proxies of climate and human settlement. Over 98% of the Plasmodium falciparum endemic world where transmission intensity exceeds 40% prevalence is located in Africa. Africa continues to bear the greatest global malaria disease burden. The MPHEG will continue to assemble temporally and spatially configured empirical information on malaria infection prevalence, intervention coverage and funding.

Plasmodium falciparum infected erythrocytes express on their surface, members of a diverse family of parasite molecules called PfEMP1 that are encoded by a family of 60 var genes in every parasite genome. These molecules interact with the surface of host cells and mediate parasite sequestration in tissues including the brain, an important step in the pathogenesis of cerebral malaria. Although naturally acquired antibodies to PfEMP1 provide specific protection against the molecular variants that they recognise, PfEMP1 are often considered too diverse to be vaccine candidates.

In parallel, we (Dr. Eunice Nduati, Agnes Gwela, Britta Urban) determine the phenotype and function of B cells in response to infected red blood cells using an in vitro activation assay and flow cytometry in healthy children and adults and in children with acute malaria and after convalescence. The aim of this study is to elucidate the defect that underlies the short-lived nature of antibody responses to many parasite antigens in children living in endemic areas. We have shown that memory B cells to the parasite can be detected in children for at least four months after an acute malaria episode indicating that memory B cells are generated and maintained.