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This review summarizes the roles of L and L viral proteins in TMEV-induced demyelination, an important animal model for multiple sclerosis.
Theiler’s original (TO) subgroup strains of Theiler’s murine encephalomyelitis virus (TMEV) cause a milder polioencephalomyelitis followed by virus persistence and demyelination in the spinal cords of mice. TMEV-induced demyelination is the representative of virus-induced demyelination and serves as an excellent animal model for multiple sclerosis, because of the resembling pathological features. Two non-structural viral proteins, leader (L) and L*, are reported to play an important role in TMEV biological activities. The present review will describe their properties, biological activities and how those proteins regulate TMEV-persistence, which induces the demyelinating disease. (Clin. Exp. Neuroimmunol. doi: 10.1111/j.1759-1961.2011.00021.x, September 2011)
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Himeda et al. (2011) studied this question.
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