Speaker
Description
Multiple selective pressures drive evolution of malaria parasite, and determine its phenotypic traits, like virulence, transmissibility, drug resistance, as well as its population structure in host communities. Immune regulation plays an important part in this process, both within-host and on population level. The key to parasite survival within host is its antigenic variation, whereby parasite can avoid immune clearing by switching on and off multiple antigenic variants. In P. falciparum species, this process is controlled by a multigene var family, expressed on infected erythrocytes.
To study within-host parasite- immune interactions and the resulting selection processes we develop an agent based approach, that accommodates most salient features of malaria infection - RBC depletion, immune stimulation and clearing, antigenic variation.
In out setup, each parasite strain has a specific genetic makeup (collection of var genes), drawn from a large pool. Multiple strains of such quasi-species, compete within-host via cross-reactive immunity. Furthermore, mixed stains can recombine in mosquito agent to produce new types. Parasite diversity in host population can change in response to external factors, intensity of transmission and host immune status.
We apply our model to examine individual and population level outcomes, and quantify the relationship between environmental inputs (intensity of transmission, immune competence), and the evolution of parasite population structure.
