One unifying thread running through a number of the papers on intracellular protozoa deserves special comment. This is the ever-increasing evidence that all those studied, the amastigotes of Leishmania, the erythrocytic stages of Plasmodium, and the tachyzoites of Toxoplasma, all have special ways to modify their host cells, presumably to make them more suitable for development of the parasite. At least two of the surface proteins of Leishmania turn out to be active enzymes of adaptive value, one an acid phosphatase and the other a protease. These may play roles in enabling Leishmania to develop within the sandfly gut and a phagolysosome of the mammalian macrophage. For Plasmodium falciparum developing in human erythrocytes there is good evidence that it produces a number of specific proteins that are transported through the red cell cytoplasm and come to lie just beneath or within the red cell membrane. The best studied example is the histidine-rich knob protein essential for formation of the knob-like surface structures that function in the sequestration of infected cells in capillaries of deep organs, in this way protecting them from destruction in the spleen. Some malarial proteins are also secreted into the external medium, but their function is not understood.
KeywordsPlasmodium Falciparum Parasitic Protozoan Trypanosoma Cruzi Parasitophorous Vacuole Protozoal Infection
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