Resilience and variability in pathogens and hosts.
Adaptability by means of phenotype variability in host-pathogen systems is studied using a model that resembles a class of array systems known as cellular automata. Each automaton in this model is characterized by a network of n x m processors that process the information contained in levels 0 to m. The effect of the automaton's architecture on its ability to satisfy variations in constraints is analysed, and automata-evolution experiments are described. Increasing the number of organization levels in the automaton is shown to increase its efficiency in buffering external changes, and the mechanism of modulating the processing rules appears more efficient than the mechanism of controlling the mutation rate. Analogy with biological systems suggests that hosts and pathogens evolve towards increasing modulation of their genomic information processing and that single mature lymphocytes should be able to generate more than one antigen receptor. These hypotheses can provide an explanation for the sequential ordered expression of different antigen genes in trypanosomes, as well as for immunosuppression and autoimmune phenomena.
D000818:Animals; D000940:Antigenic Variation; D005075:Biological Evolution; D006790:Host-Parasite Interactions; D008957:Models, Genetic; D008962:Models, Theoretical; D009154:Mutation; D010641:Phenotype