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American Journal of Pathology, Vol 116, 30-45, Copyright © 1984 by American Society for Investigative Pathology

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Remyelination during remission in Theiler's virus infection

MC Dal Canto and RL Barbano

Inoculation of the cell-adapted WW strain of Theiler's virus into mice produces a chronic demyelinating infection of the central nervous system (CNS) characterized by a remitting relapsing course. During remission, extensive remyelination of spinal cord white matter is observed. Remyelination is carried out by both Schwann cells and oligodendrocytes. This paper examines the possible mechanisms of entry of Schwann cells into the CNS, their possible source in different regions of the white matter, their relations with various CNS elements, and the relative activity of these cells versus that of oligodendrocytes. Observations suggest that Schwann cells, originating from peripheral roots and from perivascular areas, migrate into white matter through gaps in the glial limiting membrane ( GLM ), probably caused by active mononuclear inflammatory cells. Schwann cell invasion and axonal contact appear to be facilitated by the presence of collagen matrix along their pathway of migration. No alterations of astrocytes in the immediate vicinity of Schwann cells were observed, and free contact between Schwann cells and different neuroglial elements was present in the initial stages of Schwann cell migration. While Schwann cells were the predominant myelinating cells in the outer white matter, oligodendrocytes were numerous and very active in the inner portions of the spinal cord column. Although oligodendrocytes produced thinner myelin than normal, in most areas essentially complete remyelination by these cells was observed. These results contrast with those of previous studies of DA infected mice in which remyelination is sporadic in the presence of unabated inflammation which continues without remission for many months after infection. It is suggested that oligodendroglial cells are quite capable of extensive remyelinating activity in this infection, provided the noxa responsible for myelin injury subsides. The host inflammatory response appears to be the most likely noxa impeding remyelination in this model.