Key result
EMC-D virus inoculation causes neuronal degeneration, demyelination, and hind limb paralysis in ~60% of mice.
Infection of DBA/2 mice with the D variant of encephalomyocarditis virus causes progressive CNS lesions including neuronal degeneration and demyelination, leading to hind limb paralysis.
Provides a murine model for EMCV-induced CNS demyelination and paralysis; leaves open translation to human disease.
The central nervous system (CNS) of DBA/2 mice inoculated i.p. with the D variant of encephalomyocarditis virus (EMC-D) (10(3) PFU/head) was examined up to 28 days postinoculation (28 DPI). The virus titer of CNS reached a maximum level at 4 DPI, and infectious viruses became undetectable by 28 DPI. Histopathologically, degeneration of neurons with virus antigens was observed in St. pyramidale hippocampi, Nuc. amigdaloideus corticalis and St. granulosum cerebelli of the brain and in Cornu ventrale of the thoracic to lumbar spinal cord at 6 DPI. In addition, in the spinal cord, demyelination was found in Funiculus ventralis and Funiculus lateralis at 6 DPI and it progressed to form spongiosis at 10 DPI. In correspondence with these virological and histopathological findings, hind limb paralysis developed in some mice at 6 DPI, and its incidence increased markedly to about 60% at 10 DPI.
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Takeda et al. (1991) studied Encephalomyocarditis virus (EMC-D) infection. D variant of encephalomyocarditis virus (EMC-D) was evaluated on Hind limb paralysis at 10 days postinoculation. Inoculation of DBA/2 mice with the D variant of encephalomyocarditis virus caused neuronal degeneration, demyelination, and hind limb paralysis in approximately 60% of mice at 10 days.
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