There are two models of CNS demyelination used in our laboratory. One relies on a viral infection which targets the oligodendrocyte, the cell which synthesizes and maintains CNS myelin.
Infection produces an acute disease with myelin loss.
When the immune response to the virus is unable to provide complete immunity, the virus establishes a persistent infection. It uses the ability of the bodies own immune cells to attack target antigens of the oligodendrocyte and thereby produce demyelination. In the virus-induced disease the ability of the virus to persist is due to a fine balance in regulation of the immune response. By contrast a weak immune response results in persistence and chronic demyelination. Mice rendered genetically deficient in genes involved in the immune response are also being examined.