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Experimental demyelination produced by the A59 strain of mouse hepatitis virus
Abstract:
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 Epon-embedded 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.
Insights
Mouse hepatitis virus (MHV) infection in mice causes a biphasic illness, leading to demyelination. This MHV-A59 model offers a system for studying virus-induced demyelination.
Area of Science:
- Neuroscience
- Virology
- Immunology
Background:
- Murine coronavirus, mouse hepatitis virus (MHV), causes significant neurological disease in mice.
- MHV-A59 strain is known to induce central nervous system (CNS) infections.
Purpose of the Study:
- To characterize the biphasic disease course and neuropathology induced by MHV-A59 in C57BL/6 mice.
- To establish MHV-A59 as a model for studying virus-induced demyelination.
Main Methods:
- Intracerebral inoculation of C57BL/6 mice with MHV-A59.
- Histopathological analysis using Epon-embedded toluidine-blue staining and electron microscopy.
- Virus culture, antigen detection via immunofluorescence (IF), and antibody detection in serum.
Main Results:
- MHV-A59 infection resulted in a biphasic disease: acute hepatitis and meningoencephalitis followed by subacute spastic paralysis.
- Demyelinating lesions were observed in the brain and spinal cord.
- Virus was cultured during the acute phase but not the chronic stage; viral antigen and antibodies were detectable for extended periods postinfection.
Conclusions:
- MHV-A59 infection in mice induces biphasic neurological disease with demyelination.
- The MHV-A59 model is suitable for further investigation of virus-induced demyelination mechanisms.