A model of auto immune response.

BACKGROUND: In this work, we develop a theoretical model of an auto immune response. This is based on modifications of standard second messenger trigger models using both signalling pathways and diffusion and a macro level dynamic systems approximation to the response of a triggering agent such as a virus, bacteria or environmental toxin. RESULTS: We show that there, in general, will be self damage effects whenever the triggering agent's effect on the host can be separated into two distinct classes of cell populations. In each population, the trigger acts differently and this behavior is mediated by the nonlinear interactions between two signalling agents. CONCLUSION: If these interactions satisfy certain critical assumptions this will lead to collateral damage. If the initial triggering agent's action involves any critical host cell population whose loss can lead to serious host health issues, then there is a much increased probability of host death. Our model also shows that if the nonlinear interaction assumptions are satisfied, there is a reasonable expectation of oscillatory behavior in host health; i.e. periods of remission.

A theoretical model of the West Nile Virus survival data.

BACKGROUND: In this work, we develop a theoretical model that explains the survival data in West Nile Virus infection. RESULTS: We build a model based on three cell populations in an infected host; the collateral damage cells, the infected dividing cell, and the infected non-dividing cells. T cell-mediated lysis of each of these populations is dependent on the level of MHC-1 upregulation, which is different in the two infected cell populations, interferon-gamma and free virus levels. CONCLUSIONS: The model allows us to plot a measure of host health versus time for a range of initial viral doses and from that infer the dependence of minimal health versus viral dose. This inferred functional relationship between the minimal host health and viral dose is very similar to the data that has been collected for WNV survival curves under experimental conditions.