The authors present the results of studying encephalomyelitis caused by the neurotropic (IHM) strain of the murine hepatitis virus in 60 mice of the C3H line infected intracerebrally at the age of 4 weeks. Morphological examinations of the brain carried out on the 5th-13th day (the acute period) and the 14th-30th day (the subacute stage) have shown that it is myelin-producing cells that are affected first in this form of encephalomyelitis, while the periaxonal process observed is a consequence of this affection. Proofs of this conclusion are presented. It is shown that in subacute encephalomyelitis, similar processes develop. Degeneration and infection of oligodendrocytes are not so pronounced in that case, as in the acute disease. However, destruction of even individual oligodendrocytes may lead (due to the peculiarities of their structure and function) to an avalanche-like process of demyelinization. It is supposed that the vesicular degeneration of myelin may arise in the sites of close contact between the myelin membranes and the cells of inflammation infiltrates (release of lysosomal enzymes and toxic products formed in edema). In the latter case the viruses serve as an antigen depot that causes and maintains the inflammatory process.