• 1 January 1979
    • journal article
    • research article
    • Vol. 40  (3) , 324-330
Abstract
Newborn ICR mice were infected by intracerebral inoculation of 105.3 LD50 of the WW strain of Theiler''s virus and examined serially by virologic and ultrastructural methods. Maximal titers of 106 LD50 developed in the brain by day 8 when 90% of the animals were dead or moribund. The virus first appeared and was most prominent in the thalamus, basal ganglia and midbrain. It spread from these areas throughout the cortex, brainstem and spinal cord but spared the cerebellar cortex. Both neurons and oligodendroglia were infected. Infected cells first showed dispersion of polyribosomes, accumulation of vesicles and widening of perinuclear cisternae. Normal cytoplasmic organelles and the nucleus were displaced by an accumulation of viral crystals, membranous profiles and fibrillar material. Within degenerating cells the nuclear chromatin became clumped and marginated and the cytoplasm was filled either with vesicles or masses of paracrystalline viral arrays. These changes were accompanied by a vigorous inflammatory response of lymphocytes, plasma cells, macrophages, neutrophils and eosinophils. Lysis of oligodendroglia during acute infection with the WW strain of Theiler''s virus may provide a stimulus for the late autoimmune demyelination that was described in animals that survive the acute encephalitis.