Microglia-mediated neuroinflammation is an amplifier of virus-induced neuropathology
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Microglia, the major resident immune cells in the central nervous system (CNS) are considered as the key cellular mediators of neuroinflammatory processes. In the past few years, microglial research has become a main focus in cellular neuroimmunology and neuroinflammation. Chronic/remitting neurological disease such as multiple sclerosis (MS) has long been considered an inflammatory autoimmune disease with the infiltration of peripheral myelin-specific T cells into the CNS. With the rapid advancement in the field of microglia and astrocytic neurobiology, the term neuroinflammation progressively started to denote chronic CNS cell-specific inflammation in MS. The direct glial responses in MS are different from conventional peripheral immune responses. This review attempts to summarize current findings of neuroinflammatory responses within the CNS by direct infection of neural cells by mouse hepatitis virus (MHV) and the mechanisms by which glial cell responses ultimately contribute to the neuropathology on demyelination. Microglia can be persistently infected by MHV. Microglial activation and phagocytosis are recognized to be critically important in the pathogenesis of demyelination. Emerging evidence for the pathogenic role of microglia and the activation of inflammatory pathways in these cells in MHV infection supports the concept that microglia induced neuroinflammation is an amplifier of virus-induced neuropathology.
KeywordsVirus-induced neuroinflammation Demyelination Axonal loss Multiple sclerosis Experimental animal model of multiple sclerosis Neuroimmunology Neurobiology of demyelinating diseases
Virus-induced experimental animal model for studying to understand the neuroinflammatory mechanism of demyelination research is supported by the Department of Biotechnology (DBT), Council for Scientific and Industrial Research (CSIR), and IISER-K, India, National Multiple Sclerosis Society, USA, M. E. Groff Surgical Medical Research and Education Charitable Trust, and Lindback Foundation Career Enhancement Award, USA. The success of this work has largely depended on the contribution and devotion of my PhD students, project students, and many collaborators whose names are listed in the references.
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