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Updated: Jun 18, 2026
Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis
Published on: October 13, 2023
Neuropathogenesis of Theiler's murine encephalomyelitis virus infection, an animal model for multiple sclerosis
Ikuo Tsunoda1, Robert S Fujinami
1Department of Pathology, University of Utah School of Medicine, 30 North 1900 East, 3R330 SOM, Salt Lake City, UT 84132, USA. itsuno@lsuhsc.edu
Abstract:
Theiler's murine encephalomyelitis virus (TMEV) infection of mice is an experimental model for multiple sclerosis (MS). TMEV induces a biphasic disease in susceptible mouse strains. During the acute phase, 1 week after infection, TMEV causes polioencephalomyelitis characterized by infection and apoptosis of neurons in the gray matter of the brain. During the chronic phase, about 1 month after infection, virus infects glial cells and macrophages, and induces inflammatory demyelination with oligodendrocyte apoptosis and axonal degeneration in the white matter of the spinal cord. Although antibody, CD4(+), and CD8(+) T cell responses against TMEV capsid proteins play important roles in neuropathogenesis, infectious virus with persistence is necessary to induce demyelination; in general, adoptive transfer of antibody or T cells alone did not induce central nervous system (CNS) disease. The TMEV model can be useful for testing new therapeutic strategies specifically as a viral model for MS. Therapies targeting adhesion molecules, axonal degeneration, and immunosuppression can be beneficial for pure autoimmune CNS demyelinating diseases, such as experimental autoimmune encephalomyelitis, but could be detrimental in virus-induced demyelinating diseases, such as progressive multifocal leukoencephalopathy.
Insights
Theiler's murine encephalomyelitis virus (TMEV) infection in mice serves as a model for multiple sclerosis (MS). Persistent TMEV infection, not just immune responses, is crucial for inducing demyelination in the central nervous system (CNS).
Area of Science:
- Neuroscience
- Virology
- Immunology
Background:
- Theiler's murine encephalomyelitis virus (TMEV) infection in mice is a valuable experimental model for studying multiple sclerosis (MS).
- TMEV infection exhibits a biphasic disease course in susceptible mouse strains, involving distinct pathological processes in the acute and chronic phases.
Purpose of the Study:
- To elucidate the role of persistent TMEV infection versus immune responses in the development of central nervous system (CNS) demyelination.
- To highlight the utility of the TMEV model for evaluating therapeutic strategies for viral-induced demyelinating diseases.
Main Methods:
- Induction of TMEV infection in susceptible mouse strains.
- Analysis of viral persistence, immune cell infiltration (CD4+ and CD8+ T cells), and neuropathological changes (neuronal apoptosis, demyelination, axonal degeneration) in the CNS.
- Assessment of the effects of adoptive transfer of antibodies or T cells on disease induction.
Main Results:
- Acute TMEV infection causes polioencephalomyelitis with neuronal apoptosis.
- Chronic infection leads to inflammatory demyelination, oligodendrocyte apoptosis, and axonal degeneration in the spinal cord.
- Persistent infectious virus, not solely antibody or T cell responses, is necessary for inducing demyelination; adoptive transfer of immune cells alone did not cause CNS disease.
Conclusions:
- The TMEV model is critical for understanding viral-induced demyelination and for testing therapies targeting CNS diseases.
- Therapeutic strategies effective for autoimmune demyelination may be detrimental in virus-induced demyelinating conditions, emphasizing the need for model-specific treatment approaches.
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