Session 2C: Inaugural Lectures by Fellows/Associates

Rajiva Raman, Varanasi

Mouse Hepatitis Virus-induced Neuroinflammation in an Experimental Animal Model Helps Better Understand the Complex Mechanism of Human Demyelinating DiseaseMultiple Sclerosis.

Myelin forms an insulating sheath surrounding axons/neurons in the nervous system, essential for rapidly propagating neuronal action potentials. Demyelination is an acquired neurodegenerative disorder where myelin degenerates, resulting in dysfunction of normal neuron-to-neuron communication and, in many cases, varying degrees of axonal degeneration. Multiple Sclerosis (MS) is the most common neuroinflammatory demyelinating disorder in young adults. Though demyelination is the primary manifestation, studies have clearly documented concomitant axonal loss to varying degrees resulting in long-term disability. Axonal injury may occur secondary to myelin damage (outside-in model), ormyelin damage may occur secondary to axonal injury (inside-out model). Mouse hepatitis virusinduced demyelination models have provided unique insights into the cellular mechanisms of myelin destruction, illustrating mechanisms of viral persistence, latent infections, virus reactivation, and viral-induced tissue damage. These studies have also provided excellent paradigms for studying the immune and central nervous system (CNS) interactions. The current trend in CNS disease biology in our laboratory is to attempt to understand the neural-cell–immune interaction to investigate the underlying mechanism of neuroinflammation rather than focusing on peripheral immune activation. Our studies delineate the potential cellular, molecular, and immunological mechanisms of CNS axonal loss and demyelination in a viral-induced mouse model of MS.