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Infection of class II-deficient mice by the DA strain of Theiler's virus
L Fiette1, M Brahic, C Pena-Rossi
1Unité des Virus Lents, URA 1157 Centre National de la Recherche Scientifique, Institut Pasteur, France.
Abstract:
The DA strain of Theiler's virus causes, in susceptible strains of mice, a persistent infection of the white matter of the spinal cord accompanied by chronic inflammation and primary demyelination. In resistant strains, including all H-2b strains, mice clear the infection after 1 to 2 weeks. We inoculated RHAbetao/o mice, an H-2b strain which does not express class II molecules. We found that they are susceptible to persistent infection and that they develop foci of chronic inflammation with demyelination. However, these foci are smaller and contain fewer demyelinated axons than those observed in susceptible SJL/J or beta2m-/- mice.
Insights
Theiler
Area of Science:
- Neuroimmunology
- Virology
- Immunogenetics
Background:
- Theiler's virus (TMEV) infection causes central nervous system (CNS) demyelination.
- Susceptibility to persistent TMEV infection is linked to specific mouse strains, particularly those not expressing H-2b.
- Class II molecule expression is considered crucial for clearing TMEV infection.
Purpose of the Study:
- To investigate the role of class II molecules in TMEV-induced demyelination.
- To determine if H-2b mice lacking class II expression are susceptible to persistent TMEV infection.
- To characterize the resulting neuropathology in these mice.
Main Methods:
- Inoculation of RHAbetao/o mice (H-2b strain lacking class II expression) with Theiler's DA virus.
- Assessment of viral clearance, inflammation, and demyelination in the spinal cord.
- Comparison of neuropathological findings with susceptible (SJL/J) and beta2m-/- mice.
Main Results:
- RHAbetao/o mice, despite being H-2b, developed persistent TMEV infection.
- These mice exhibited chronic inflammation and demyelination in the spinal cord white matter.
- The observed demyelinating lesions were smaller and had fewer demyelinated axons compared to susceptible control groups.
Conclusions:
- Class II molecule expression is not essential for developing persistent TMEV infection and demyelination.
- Absence of class II molecules may lead to a less severe neuropathological outcome.
- This suggests alternative immune mechanisms or pathways contribute to viral clearance and lesion development.