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Malaria parasites cause disease only in their blood stage, i.e., when they settle and proliferate in red blood cells. Then fatal complications may develop, albeit virtually exclusively in infections with Plasmodium falciparum. The main reason is that P. falciparum in a complicated process transports some of its own proteins onto the surface of the infected red blood cell and makes it stick to the wall of a small blood vessel. Thereby, the parasites impair the microcirculation and may give rise to fatal organ failure, in particular upon attachment in blood vessels of the brain. The advantage for the parasites is that, by hiding the periphery, they avoid the circulation and escape being trapped in the spleen, which culls red blood cells carrying chunky loads such as haemoglobin precipitates or malaria parasites. Thus, P. falciparum is able to develop particularly fast and numerously by hiding in small blood vessels.
The value of animal models for studying human infectious diseases is increasingly being questioned. Nonetheless, it remains a serious disadvantage if no appropriate animal model is available at all, and this applies particularly to the life-threatening complications of human malaria.
As the proteins produced by P. falciparum to attach infected red blood cells to a vessel wall are located on the outer cell surface (p. 55), they are recognised by our immune cells, resulting in the production of antibodies, which may inhibit attachment
Many of the surface molecules of blood vessels used by Plasmodium falciparum to attach its red blood cell are present in the vessels of certain organs only. Therefore, it happens that only a single organ is affected at a given time of a P. falciparum infection. We have expressed some of these surface molecules of human blood vessels on hamster cells.