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Natural immunity against malaria is acquired after repeated infections for an extended period of time resulting in a state of immunological non-responsiveness against the malaria parasite. This state ultimately prevents the onset of severe disease such as cerebral malaria thereby reducing the risk of death from malaria. Individuals with acquired natural immunity to malaria still harbor parasites (albeit in low densities) in the blood, and therefore natural immunity against malaria is not sterile. For this reason, natural immunity to malaria cannot be compared to immunity achieved against other diseases where the immune response neutralizes and eliminates the pathogen. The second hallmark of natural immunity to malaria is that protection wanes once a “protected” individual leaves the malaria-endemic area indicating that protection depends on continued antigen exposure. Immunity to malaria is stageand species-specific and distinct immune mechanisms confer protection against the different developmental stages of the parasite. In the case of blood stage infection, passive transfer experiments with purified human immunoglobulins derived from immune individuals living in malaria-endemic areas have demonstrated that antibodies can mediate protection (Cohen et al., 1961; Butcher et al., 1970; BouharounTayoun et al., 1990). Mechanistic studies revealed that the effect of blood stage-specific antibodies on the asexual erythrocytic parasite depends on their antigen-specificity; antibodies can bind to merozoites, opsonize and target them towards phagocytic cells of the host (Groux and Gysin, 1990), or prevent invasion of new erythrocytes (Perkins, 1991). Once infected, antibodies against asexual blood stage antigens such as Pf332 or MSP-1 inhibit the intra-erythrocytic development of Plasmodium falciparum (Ahlborg et al., 1996; Siddique et al., 1998; Bergmann-Leitner et al., 2009). Antibodies directed to antigens expressed by sexual erythrocytic stages (gametocytes) have been shown to prevent transmission of malaria by blocking either the infection of the mosquito or the development in the mosquito (Lavazec and Bourqouin, 2008). As will be outlined in this chapter, it becomes increasingly clear that a blood stage vaccine may never be able to induce sterile protection, but can prevent mortality. Why bother developing blood stage vaccines? Extensive studies characterizing

The Impact of Immune Responses on the Asexual Erythrocytic Stages of Plasmodium and the Implication for Vaccine Development