Inflammation and Demyelination in the Central Nervous System International Congress of Neuropathology, Vienna, September 5–10, 1982

The present report, compares two murine models of virus induced chronic relapsing demyelination. MHV-induced demyelination in the BALB/c mouse results from the direct virus mediated cytolysis of oligodendrocytes. Extensive remyelination by oligodendrocytes is noted. Recurrent demyel­ ination occurs in small areas. Infectious virus persists and 34 Fig. 2: Demyelination in SJL/J mice infected with TMEV. A) Multifocal areas of perivascular demyelination in the spinal cord (110 days post infection). Para­ phenylene diamine stain. X 250. B) Perivascular inflammatory infiltration within the white matter of the spinal cord (22 days post infec­ tion). Paraphenylene diamine stain. X600. C) Localization of TMEV associated antigen in the cytoplasm of oligodendrocytes (45 days post infec­ tion). Vibratome section stained with the peroxidase-anti peroxidase technique. X 400. D) Immunoperoxidase staining of viral antigen within inner and outer loops of an oligodendrocyte (45 days post infectin) X 60,000. E) Longitudinal section showing viral antigen within Schmidt-Lanterman incisures (80 days post infection). X 49,000. viral antigens are localized within oligodendrocytes and their processes. TMEV-induced demyelination in SJL/J mice is asso­ ciated with perivascular inflammatory infilrates and is dimin­ ished by immunosuppressive measures. Remyelination by oligo­ dendrocytes is delayed and incomplete. Chronic demyelination is widespread and associated with perivascular inflammatory infiltrates. The virus persists and viral antigen is local­ ized within oligodendrocytes.