Key result
Inoculation of rats with EMC-D virus caused acute meningoencephalitis in animals younger than 14 days, while no viral replication or lesions were detected in those inoculated at 28 and 56 days.
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The susceptibility of rat brain to encephalomyocarditis virus infection decreases with age, likely reflecting changes in neuronal susceptibility and immune system maturation.
Rats were inoculated intraperitoneally (i.p.) or intracerebrally (i.c.) with 1 x 10(4) plaque forming units (PFU)/animal of the D variant of encephalomyocarditis virus (EMC-D) at 2, 4, 7, 14, 28 or 56 days of age for virological and histopathological examination. In the i.p.-inoculation study, neither viral replication nor lesions were detected in the animals inoculated at 28 and 56 days of age. In the animals inoculated when younger than 14 days of age, lesions were restricted to the brain although viral replication was detected in the brain, heart and pancreas. The brain lesions were characterized by acute meningoencephalitis with neuronal necrosis in the cerebral cortex, hippocampus and thalamus, and viral RNA was detected in degenerated and/or intact neurons. In the i.c.-inoculation study, similar age-related changes in susceptibility of rat brain to EMC-D infection were observed, but a minor difference was that viral replication and lesions were still detected in the hippocampus of some animals inoculated at 28 days of age. These results suggest that an age-related decrease in the susceptibility of rat brain to EMC virus infection may reflect an age-related change in the susceptibility of neurons themselves as well as in maturation of the immune system.
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Ikegami et al. (1997) studied Encephalomyocarditis virus infection. D variant of encephalomyocarditis virus (EMC-D) inoculation was evaluated on Viral replication and lesions. Inoculation of rats with EMC-D virus caused acute meningoencephalitis in animals younger than 14 days, while no viral replication or lesions were detected in those inoculated at 28 and 56 days.
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