Int. J. Mol. Sci. 2012, 13(6), 7365-7374; https://doi.org/10.3390/ijms13067365
Role of Microglia in Oxidative Toxicity Associated with Encephalomycarditis Virus Infection in the Central Nervous System
1
Central Laboratories for Frontier Technology, Kirin Holdings Co, Ltd, 1-13-5 Fukuura Kanazawa-ku, Yokohama-shi, Kanagawa 236-0004, Japan
2
Laboratory of Biometabolic Chemistry, School of Health Sciences, Faculty of Medicine, University of the Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan
3
Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan
*
Author to whom correspondence should be addressed.
Received: 2 May 2012 / Revised: 28 May 2012 / Accepted: 5 June 2012 / Published: 14 June 2012
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Abstract
The single-stranded RNA encephalomyocarditis virus (EMCV) can replicate in the central nervous system (CNS) and lead to prominent brain lesions in the stratum pyramidale hippocampus and the stratum granulosum cerebelli. Activated microglia cells infected by EMCV produce a massive burst of reactive oxygen species (ROS) via NADPH oxidase 2 (NOX2) activation, leading to neuronal death. Balancing this effect is mechanisms by which ROS are eliminated from the CNS. Cellular prion protein (PrPC) plays an important antioxidant role and contributes to cellular defense against EMCV infection. This review introduces recent knowledge on brain injury induced by EMCV infection via ROS generation as well as the involvement of various mediators and regulators in the pathogenesis. View Full-TextKeywords:
encephalomyocarditis virus (EMCV); reactive oxygen species (ROS); NADPH oxidase (NOX); microglia
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).
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Ano, Y.; Sakudo, A.; Onodera, T. Role of Microglia in Oxidative Toxicity Associated with Encephalomycarditis Virus Infection in the Central Nervous System. Int. J. Mol. Sci. 2012, 13, 7365-7374.
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