Abstract
Infection with Theiler’s murine encephalomyelitis virus (TMEV) provides an opportunity to study viral persistence and neuropathologic abnormalities in the central nervous system. This picornavirus was first recovered by Max Theiler in 1934 from a mouse suffering from spontaneous flaccid paralysis of the hind legs (Theiler, 1934). The virus is similar in size, virulence, buoyant density and viral structural proteins to poliovirus (Lorch et al., 1981). Early studies showed that intracerebral or intranasal inoculation of the virus into neonatal or weanling mice resulted in spinal cord lesions characterized by neuronal necrosis, especially of anterior horn cells, which is very similar to human poliomyelitis. This virus received little attention until Daniels et al. (1952) described an isolate of TMEV, subsequently designated DA strain, which had the propensity to induce in young adult mice primary demyelination in the central nervous system. The pathology in the spinal cord was characterized by an intense inflammatory infiltrate associated with primary destruction of myelin sheaths with relative preservation of axons (Dal Canto and Lipton, 1975; Lehrich et al., 1976).
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Rodriguez, M., David, C.S., Pease, L.R. (1987). The Contribution of MHC Gene Products to Demyelination by Theiler’s Virus. In: David, C.S. (eds) H-2 Antigens. NATO ASI Series, vol 144. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0764-9_72
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DOI: https://doi.org/10.1007/978-1-4757-0764-9_72
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