Modelling the immune response to malaria with ecological concepts: short-term behaviour against long-term equilibrium.
A model for the human immune response to the malaria parasite Plasmodium falciparum is used to analyse the dynamics of an infection within an individual patient. Previous models either looked at competition between two parasite genotypes or at one parasite clone and the immune response to it. This model describes the course of an infection caused by the blood stages of two parasite genotypes differing in reproductive rate and in the immune response they elicit. The interactions between the genotypes can be interpreted as exploitative competition for red blood cells. Interactions between omnipotent immune cells and parasites resemble a predator-prey relation. In analysing these kinds of models, classical theoretical ecology usually deals with long-term behaviours, i.e. looks for equilibria and conditions for coexistence. However, especially in endemic regions with ongoing transmission, an equilibrium state of infections is unlikely. When reinfections with another parasite genotype were considered, the short-term dynamics of the infection changed dramatically, depending on which genotype was first, when the second one appeared, and what kind of immune response was elicited. If the slow development of immunity to malaria really is due to its genotype specificity, the effects of superinfections will be of great importance.
Hellriegel
B
B
Zoologisches Institut Basel, Switzerland.
D000818:Animals; D004463:Ecology; D004912:Erythrocytes / Q000469:parasitology; D005838:Genotype; D016778:Malaria, Falciparum / Q000097:blood / Q000276:immunology*; D008433:Mathematics; D008954:Models, Biological; D010963:Plasmodium falciparum / Q000235:genetics / Q000276:immunology