IISER MOHALI

Abstract: Multiple Sclerosis (MS) is an immune-mediated demyelinating disease concurrent with or without axonal loss of the central nervous system of humans. Although the etiology of MS is enigmatic, underlying elements contributing to disease development include genetic and environmental factors. Recent epidemiological evidence has pointed to viral infection as a trigger for initiating white matter damage in the human CNS. Mouse hepatitis virus (MHV) is a β-Coronavirus, a positive-strand RNA virus that, following intracranial infection of susceptible C57BL/6 mice, induces an acute encephalomyelitis that later resolves into a chronic progressive demyelinating disease that mimics certain pathological and clinical features of human neurological disease MS. CNS resident Neuroglial cells' interaction with peripheral infiltrating immune cells into the panglial system is critical to suppress viral replication and clearance of the viral particles but initiate demyelination. Recent efforts by our laboratory and others have focused on strategies to understand the host cell factor involved in the neuroinflammation process and design the antivirals against murine β-Coronavirus infection. The talk will focus on understanding the cellular and molecular aspects of the biology of the mouse hepatitis virus (MHV) induced neuroinflammation and demyelination, which provides essential insights into the underlying pathophysiology of demyelination and axonal loss in MS.