Related Experiment Videos
Primary demyelination in Theiler's virus infection. An ultrastructural study
Abstract:
Theiler's virus infection in SJL/J mice was studied ultrastructurally at subsequent intervals after intracerebral inoculation. Extensive spinal cord lesions consisting of leptomeningeal and white matter mononuclear cell infiltrates with concomitant primary demylination were seen by 15 days. Stripping of myelin lamellae by invading mononuclear cell processes and vesicular disruption of myelin were demonstrated to be the patterns of myelin breakdown. Oligodendrocytes in the vicinity of demyelinating lesions never showed degenerative changes, and viral inclusions could not be found in any cells in the central nervous system. Remyelinating axons, first detected 21 days after infections, were more frequently seen in the late phase of the disease when conspicuous gliosis was also present. Active demyelination could still be observed as late as one year after infection at which time inflammation was decreased. However, plasma cells were relatively more numerous at later times after infection. These ultrastructural findings are similar to experimental allergic encephalomyelitis, and suggest an immune-mediated mechanism of demyelination in Theiler's virus infection.
Insights
Theiler's virus infection causes spinal cord demyelination in mice, characterized by myelin breakdown and inflammation. Findings suggest an immune-mediated mechanism similar to experimental allergic encephalomyelitis.
Area of Science:
- Neuroscience
- Immunology
- Virology
Background:
- Theiler's virus is a murine model for studying central nervous system inflammation and demyelination.
- Understanding the pathogenesis of Theiler's virus infection is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the ultrastructural changes in the spinal cord during Theiler's virus infection.
- To elucidate the mechanism of demyelination and identify cellular players involved.
Main Methods:
- Ultrastructural analysis (electron microscopy) of spinal cord tissue from infected SJL/J mice at various time points.
- Observation of cellular infiltrates, myelin breakdown patterns, and glial responses.
Main Results:
- Spinal cord lesions with mononuclear cell infiltrates and primary demyelination were observed by 15 days post-infection.
- Myelin breakdown occurred through lamellar stripping and vesicular disruption by mononuclear cell processes.
- Oligodendrocytes showed no direct degenerative changes, and viral inclusions were absent in CNS cells.
- Remyelination and gliosis were evident in later stages, with active demyelination persisting for up to a year.
- Plasma cells increased in later stages, while overall inflammation decreased.
Conclusions:
- The ultrastructural pathology of Theiler's virus infection resembles experimental allergic encephalomyelitis.
- Findings strongly suggest an immune-mediated mechanism underlying demyelination in this viral model.
- The study provides insights into the chronic inflammatory and demyelinating processes in the central nervous system.