Speakers
Description
Ordinary differential equation (ODE) models of the pathogenesis of multiple sclerosis (MS) were made to study the role of EBV infection on MS dynamics. Modeling allows in silico testing of several hypotheses regarding the role of EBV on MS pathogenesis and the efficacy of anti-viral therapies and anti-EBV vaccines.
Two ODE models were made, one of the immune system, and the other of CNS damage. The immune system model assumes that dysregulation caused by EBV infection causes spikes in the population of T-effector cells. The populations of T-effector, Active B, and Infected B cells from the immune system model are consolidated into the CNS model, representing inflammation that causes axon damage.
In order to test various hypotheses of the mechanism by which EBV causes MS, various parameters were manipulated to see the effects on the levels of the T-eff population. The hypotheses that were tested were molecular mimicry, mistaken self, bystander damage, insufficient killing of infected B-cells by Natural Killer cells, and EBV induced B cell migration to CNS.
Furthermore, antiviral therapies, vaccines, and existing MS therapies were incorporated to test the effects on T-effector and B-cell populations. The existing MS therapies were used to further constrain the models, as well as to predict the effects of combinations of therapies. These models show that there are multiple mechanisms that can manifest in the inflammation that causes MS symptoms.
