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From the Multiple Sclerosis Research Center of the Wistar Institute of Anatomy and Biology (Drs. Lavi, Gilden, and Wroblewska), and the Departments of Neurology (Drs. Lavi and Gilden), Microbiology (Qr. Weiss), and Pathology (Dr. Rorke), University of Pennsylvania School of Medicine, Philadelphia, PA.
Intracerebral inoculation of 4- to 6-week-old C57BL/6 mice with the A59 strain of mouse hepatitis virus (MHV), a murine coronavirus, produced biphasic disease. Acute hepatitis and mild meningoencephalitis were followed by subacute spastic paralysis with demyelinating lesions in the brain and spinal cord as determined by Eponembedded toluidine-blue-stained sections and by electronmicroscopy. MHV-A59 was cultured by plaque assay from the blood, brain, spinal cord, and liver of infected mice during the acute phase, but not in the chronic stage. MHV-A59 antigen was detected by immunofluorescence (IF) until 3 months postinfection (PI). Serum anti-MHV-A59 antibodies were detected from 7 days to 5 months PI. The induction of demyelination by MHV-A59 provides a suitable system to study virus-induced demyelination further.
Address correspondence and reprint requests to Dr. Lavi, Department of Neurology, Hospital of the University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104.
This work was supported by grants RG-1421-A-1 and RG-894-C3 from the National Multiple Sclerosis Society and grants A1 17418 and NS 11037 from the National Institutes of Health. Dr. Lavi was the recipient of a Penn-Israel Wexler Fellowship award and was supported in part by the Kroc Foundation.
Presented at the 35th meeting of the American Academy of Neurology, San Diego, CA, April 1983.
Accepted for publication August 17, 1983.
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