The art of parasite survival.
Parasites develop and survive in an environment which is often hostile to them. When facing aggressive conditions parasites are able to use various and complex strategies. Echinococcus granulosus, Toxocara canis, Pneumocystis carinii, Entamoeba or Toxoplasma gondii are able to seclude from the environment when stressed by surrounding (immunologic or non-immunologic) aggressive factors. Specific antigens which exert a functional activity during a short period of time appear to be concealed from the immune attack at this crucial moment. This is the case for rhoptry or dense granule antigens of Plasmodium or Toxoplasma sporozoa involved in the formation of the parasitophorous vacuole which are released in a space perfectly isolated from the outside and therefore from antibodies. Some parasites like Schistosoma mansoni or Trypanosoma brucei reveal an amazing opportunistic behavior when they use cytokines of host origin induced by the infectious process for their own development. Leishmania, Toxoplasma and Trypanosoma cruzi are able to invade immunologically competent macrophages and to avoid the triggering of killing mechanisms of these cells. Parasites also take advantage of the genetic restriction of the immune response and it has been observed for Plasmodia that some high molecular weight antigens are unable to induce an immune response in particular strains of mice. Parasite receptors involved in the invasion of host cells by parasites can function in the presence of antibodies which can explain the failure of vaccination attempts targeting this type of molecules. Among the mechanisms developed by parasites to resist to drugs it appears that transmembrane transporters described in many protozoa or helminth parasites could play a role. Moreover, the description of parasite-specific enzymes able to protect them against the damaging effects of oxygen radicals suggests that parasites are potentially able to develop a resistance phenomenon against drugs acting via an oxidative burst.
Camus
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D
INSERM U42, Biologie et Biochimie Parasitaires et Fongiques, Villeneuve d'Ascq, France.
Zalis
M G
MG
Vannier-Santos
M A
MA
Banic
D M
DM
D000222:Adaptation, Physiological; D000818:Animals; D004351:Drug Resistance; D017125:Genes, Protozoan; D006790:Host-Parasite Interactions; D006801:Humans; D051379:Mice; D010271:Parasites / Q000187:drug effects / Q000235:genetics / Q000276:immunology / Q000502:physiology*; D010963:Plasmodium falciparum / Q000235:genetics / Q000502:physiology; D011817:Rabbits; D051381:Rats