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Experimental neuropathology of chronic demyelination induced by a JHM virus variant (DS)
Abstract:
A small plaque variant of JHM virus has a markedly reduced ability to kill mice following intracerebral inoculation. Spinal cords of mice surviving 13 to 16 months following acute infection with this variant were examined ultrastructurally. Multiple subpial areas of demyelination in the anterior and lateral white matter were found in five of 13 mice. The lesions had more gliosis, fewer oligodendrocytes, and less remyelination than has been described following other infections with JHM virus. No conclusive evidence of active demyelination or viral-like particles was found. The pathogenesis of the lesions observed may be due to a persistent, attenuated infection of oligodendrocytes or to immunologic processes. These lesions were similar to chronic multiple sclerosis plaques. Therefore, this variant should prove to be a useful tool for studying the long-term effects of viral-induced demyelinating diseases.
Insights
A JHM virus variant causes less severe disease in mice, leading to demyelination similar to multiple sclerosis plaques. This offers a valuable model for studying chronic viral-induced neurological damage.
Area of Science:
- Neurovirology
- Demyelinating Diseases
- Pathogenesis
Background:
- JHM virus is a neurotropic coronavirus known to cause demyelination.
- A small plaque variant of JHM virus exhibits reduced pathogenicity in mice.
Purpose of the Study:
- To investigate the long-term ultrastructural changes in the spinal cords of mice infected with a JHM virus plaque variant.
- To assess the potential of this variant as a model for studying chronic demyelinating diseases.
Main Methods:
- Intracerebral inoculation of mice with a JHM virus plaque variant.
- Ultrastructural examination of spinal cord tissues from surviving mice (13-16 months post-infection).
Main Results:
- Five of 13 surviving mice exhibited subpial demyelination in the anterior and lateral white matter.
- Lesions showed increased gliosis, reduced oligodendrocyte numbers, and limited remyelination compared to other JHM virus infections.
- No definitive signs of active demyelination or viral particles were observed.
Conclusions:
- The observed demyelinating lesions share similarities with chronic multiple sclerosis plaques.
- The pathogenesis may involve persistent, attenuated oligodendrocyte infection or immunologic responses.
- This JHM virus variant is a promising tool for modeling long-term viral-induced demyelination.