Abstract

Blockage of cerebral microvessels by Plasmodium falciparum-infected erythrocytes appears to be the principal cause of the pathology of cerebral malaria. Knobs on infected erythrocytes act as the focal junctions of cell contact to endothelial cells. The knobs are, therefore, important in blockage of the microvascular lumen and in ensuring pathological changes in cerebral tissues. Immunological events might also play an important role in the pathogenesis of cerebral malaria. It is important to assess the candidate malaria vaccines now in development, not only for their efficacy in reducing blood parasitemia but also for any effects they have to increase or decrease the sequestration of infected erythrocytes in the brain and the attendant pathology.

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