NASOENCEPHALOPATHY OF MICE INFECTED INTRANASALLY WITH A MOUSE HEPATITIS VIRUS, JHM STRAIN

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  • 1 January 1977
    • journal article
    • research article
    • Vol. 47  (1) , 59-70
Abstract
A mouse hepatitis virus, strain JHM, grown on [mouse] DBT cells was inoculated intranasally into ICR-SLC weanling mice, and histopathological lesions were studied in relation to viral growth. In the spleen virus titer reached a peak of 103 PFU[plaque forming units]/0.2 g 48 h after inoculation, and later it decreased gradually. No virus was detected in the liver throughout the experiment, while some early inflammatory reactions appeared in the spleen and liver without any further development. At 48 h postinoculation there existed degeneration and necrosis in the nasal mucosa and submucosa. In the brain and spinal cord active viral growth was seen at 48 h postinfection or later. In the olfactory bulb mitral cells were also affected with accumulation of glial cells and some meningitis. At 72-96 h postinoculation, degeneration of neurons and glial cells were remarkable in the tructus olfactorius, cortex of lobus piriformis, septa pellucidum and commissura anterior accompanying meningitis. At 120 h postinfection, pyramidal cells in the hippocumpus were also degenerated and necrotized, and nodular proliferation and collapse of glial cells, small foci of demyelination and perivascular cuffing were seen in the interbrain. At 144 h postinoculation or later, the lesions developed through the whole brain including the pons and medulla oblongata as well as spinal cord. Brain virus titers showed 105 PFU/0.2 g at 120 h and 104 PFU/0.2 g at 144 h postinfection. In mice surviving at 168 h after inoculation, severe demyelinating lesions were observed despite a decreased virus titer. Intranasally inoculated virus might invade the olfactory bulb through the tractus olfactorius and then produce necrotizing lesions, extending later towards the posterior parts of the CNS.

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