Coronavirus Infection and Demyelination [chapter]

Helmut Wege, Hermann Schluesener, Richard Meyermann, Vesna Barac-Latas, Gerda Suchanek, Hans Lassmann
1998 Advances in Experimental Medicine and Biology  
0-17498 Isle ofRiems 2Institute of Brain Research 0-72076 Tiibingen 3Institute of Neurology A-1090 Vienna, Austria 1. ABSTRACT 55 Coronavirus infections of rodents can cause diseases of the central nervous system characterised by inflammatory demyelination. The lesions mimick in many aspects the pathology of mUltiple sclerosis in humans and of other neurological diseases. As an animal model for demyelination, we studied the MHV-JHM induced encephalomyelitis of Lewis rats. The pathomorphological
more » ... pathomorphological analysis revealed patterns of lesions which developed in stages. Infected oligodendrocytes were first destroyed by necrosis. Later stages were characterized by demyelinated plaques. In the center of plaques, no virus antigen was found and oligodendrocytes were mainly destroyed by apoptosis. At the edge of plaques, virus antigen was expressed in parallel to infiltrations consisting of lymphocytes and macrophages. The prevailing mechanisms leading to demyelination may change individually and during defined stages of the disease. The transcriptional expression of chemoattractants and other mediators of inflammation was studied by semiquantitative RT-PCR. Virus induced inflammatory demyelination was accompanied by high expression of a relatively novel cytokine, the endothelial monocyte activating polypeptide II (EMAP II). By immunocytochemistry, EMAP II was detected in parenchymal microglia located both within the lesions and in unaffected areas. Furthermore, the level of transcriptional expression of the regulatory calcium binding SIOO proteins MRP8, MRP14 and CPIO was associated with inflammatory demyelination and expression oflFN y, IL-2, TNF n, and iNOS.
doi:10.1007/978-1-4615-5331-1_55 fatcat:2fxnyzonbnhcpjdcxl5456sjei