Abstract
Coronavirus mouse hepatitis virus (MHV) strain A59 causes severe acute hepatitis, focal meningoencephalitis, and chronic demyelinating disease of the spinal cord. It serves as an experimental model for multiple sclerosis. MHV-2 causes acute hepatitis and meningitis. The pathogenesis of MHV-induced demyelination in mice is not clear and a potential mechanism of apoptosis was suggested. Previous studies showed apoptotic T cells, astrocytes, and oligodendrocytes in demyelinating areas following MHV-JHM infection (Barac-Latas et al 1997). However, the distribution of demyelination has been suggested to correlate better with macrophage infiltration than with the apoptotic cells (Wu and Perlman 1999). In the chronic demyelinating disease induced by Theiler’s virus, apoptotic astrocytes were found in demyelinating lesions (Palma et al 1999). In experimental allergic encephalitis, the disease was much milder in mice lacking Fas-Fas ligand molecules, suggesting that apoptosis plays a role in the disease (Waldner et al 1997).
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Keywords
- Demyelinating Lesion
- Mouse Hepatitis Virus
- Severe Acute Hepatitis
- National Multiple Sclerosis Society
- Experimental Allergic Encephalitis
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© 2001 Springer Science+Business Media New York
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Schwartz, T., Fu, L., Lavi, E. (2001). Programmed Cell Death in MHV-Induced Demyelination. In: Lavi, E., Weiss, S.R., Hingley, S.T. (eds) The Nidoviruses. Advances in Experimental Medicine and Biology, vol 494. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1325-4_27
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DOI: https://doi.org/10.1007/978-1-4615-1325-4_27
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