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Coronavirus Infection and Demyelination

Development of Inflammatory Lesions in Lewis Rats
  • Helmut Wege
  • Hermann Schluesener
  • Richard Meyermann
  • Vesna Barac-Latas
  • Gerda Suchanek
  • Hans Lassmann
Chapter
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 440)

Abstract

Coronavirus infections of rodents can cause diseases of the central nervous system characterised by inflammatory demyelination. The lesions mimick in many aspects the pa-thology 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 analysis revealed patterns of lesions which developed in stages. Infected oligodendrocytes were first destroyed by necrosis. Later stages were char-acterized 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 macro-phages. 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 in-duced inflammatory demyelination was accompanied by high expression of a relatively novel cytokine, the endothelial monocyte activating polypeptide II (EMAP II). By immu-nocytochemistry, 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 S100 proteins MRP8, MRP14 and CP10 was associated with inflammatory demyelination and expression of IFN γ, IL-2, TNF α, and iNOS.

Keywords

Microglial Cell Experimental Allergic Encephalomyelitis Transcriptional Expression Central Nervous System Tissue Coronavirus Infection 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1998

Authors and Affiliations

  • Helmut Wege
    • 1
  • Hermann Schluesener
    • 2
  • Richard Meyermann
    • 2
  • Vesna Barac-Latas
    • 3
  • Gerda Suchanek
    • 3
  • Hans Lassmann
    • 3
  1. 1.Institute of Diagnostic Virology, Federal Research Centre for Virus Diseases of AnimalsFriedrich-Loeffler-InstitutesIsle of RiemsGermany
  2. 2.Institute of Brain ResearchTübingenGermany
  3. 3.Institute of NeurologyViennaAustria

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