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Immunology of Theiler's murine encephalomyelitis virus infection
E L Oleszak1, J Kuzmak, R A Good
1Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, Pa 19140, USA.
Abstract:
Theiler's murine encephalomyelitis virus (TMEV) is a single-stranded RNA virus that belongs to the family of picornaviruses. Intracranial inoculation of susceptible mouse strains with TMEV results in biphasic disease, consisting of early acute disease that resembles poliomyelitis, followed by late chronic demyelinating disease that is characterized by the appearance of chronic inflammatory demyelinating lesions. Susceptibility to TMEV infection is genetically controlled by three loci: one that maps to the H-2D region of the major histocompatibility complex, one to the beta-chain constant region of the T-cell antigen receptor, and one located on chromosome 3. Both early acute and chronic late demyelinating diseases are immunologically mediated. T cells appear to play an important role in the pathogenesis of the disease. TMEV-induced demyelinating disease in mice has extensive similarities with multiple sclerosis, and it is considered one of the best experimental animal models for multiple sclerosis.
Insights
Theiler's murine encephalomyelitis virus (TMEV) causes a biphasic disease in mice, mimicking multiple sclerosis. This viral model is crucial for understanding and developing treatments for demyelinating diseases.
Area of Science:
- Virology
- Neuroimmunology
- Genetics
Background:
- Theiler's murine encephalomyelitis virus (TMEV), a picornavirus, induces a biphasic neurological disease in susceptible mice.
- The disease progresses from acute polio-like symptoms to chronic inflammatory demyelination, resembling multiple sclerosis.
- Genetic factors, including the H-2D region and T-cell receptor, control susceptibility to TMEV infection.
Purpose of the Study:
- To investigate the pathogenesis of TMEV-induced demyelinating disease.
- To explore the role of the immune system, particularly T cells, in disease development.
- To establish TMEV as a relevant animal model for multiple sclerosis research.
Main Methods:
- Intracranial inoculation of susceptible mouse strains with TMEV.
- Observation and analysis of early acute and late chronic disease phases.
- Genetic mapping of susceptibility loci.
Main Results:
- TMEV infection leads to both acute and chronic demyelinating disease.
- Disease susceptibility is genetically controlled by three distinct loci.
- Immunological mechanisms, with a significant role for T cells, mediate disease pathogenesis.
Conclusions:
- TMEV infection in mice serves as a valuable model for studying multiple sclerosis.
- The disease is immunologically mediated, highlighting the importance of T cell responses.
- Understanding the genetic control of susceptibility can inform future research.