There is a great deal of interest among malariologists about the effect of antigenic diversity on the transmission dynamics of malaria (Day and Marsh 1991). Complementing other modelling studies on this effect at a population level (Gupta et al. 1994), we explore the within-host dynamics of blood stage malaria in a single individual infected with a basket of different parasite strains. By generalising a previous model (Anderson et al. 1989) to account for this situation and calibrating it against the observed data on the time course of malaria infection, we are able to include the effects of the host immune response despite the difficulty of obtaining quantitative data on this component.

We intend to use our model to investigate the effects of different types of immune response: for example the relative success of a fast, quickly decaying strain-specific response combined with a slowly generated but persistent strain-transcending response.

We will discuss whether combinations of strain specific and strain transcending responses to a basket of infections at the blood stage of malaria account for the observed patterns of parasitaemia in malaria endemic areas.

Following Anderson et al. (1989), and similarly to Hellriegel (1992), we define x(t) as the number of uninfected erythrocytes, m(t) as the number of free merozoites and y(t) as the number of infected red blood cells. We assume that red blood cells are produced at a constant rate Λ and die at a per-capita rate μ with a mean life-span of l/μ. Free merozoites infect unparasitised cells at a rate βxm; these cells rupture after a mean time of 1/α to produce r more free merozoites.