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Differential Expression of Malaria Invasion-Associated Proteins in the porozoite: Novel Vaccination Strategy
Framework programme:
Project number:
EC contribution:
€ 587,000
24 months
Starting date:
1 June 2005

Keywords: Malaria; vaccine; liver; sporozoite; Plasmodium


In humans, sterile immunity against malaria has only been obtained after exposure to irradiated sporozoites inoculated by mosquitoes. The full repertoire of parasite antigens that underlie this protection is not known. Recently, antigens by invasion blood stage parasites have been shown to be expressed by sporozoites, which lead to the hypothesis that they might also be involved in sporozoite invasion of hepatocytes. Using the availability of suitable model systems, this project proposes to study the expression of these invasion-associated sporozoite proteins and host immunity. This information will then be used to test a suitable approach for a new malaria vaccine formulation.


The full repertoire of pre-erythrocytic antigens that underlie the sterile protection induced by irradiated sporozoites is not actually known. The three antigens investigated to date may not be responsible for induction of optimal protective responses. This would account for the difficulties encountered in reproducing this sterile long-lasting immunity by current sub-unit vaccines. It would clearly be desirable to investigate other pre-erythrocytic antigens. Such efforts to expand targets of pre-erythrocytic stage immunity are justified because the infection is at its most vulnerable between the time when sporozoites are injected and when hepatic merozoites emerge into the blood stream. During this period, there are two distinct stages, the sporozoite and infected hepatocyte, (whose numbers rarely exceed 100 in the human body) that can be attacked. The protective responses could comprise not only humoral but also cellular effector mechanisms, since this is the only time during the infection when the parasite can be found for 5 to 14 days inside a major histocompatibility complex, MHC-expressing cell. Even if sub-optimal, the appropriate immune response could fully abrogate the infection, thus preventing both pathology and transmission to another host.

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