Pathogenesis of cerebellar hypoplasia produced by lymphocytic choriomeningitis virus infection of neonatal rats. II. An ultrastructural study of the immune-mediated pathology.
Lymphocytic choriomeningitis virus, following inoculation of 4-day-old rats, produces an acute destructive but nonfatal necrosis of the cerebellum which is immunologically mediated. An ultrastructural study of the developing lesion indicated the following sequence of events: first, lymphocytic choriomengitis virions appear in the intercellular spaces of apparently normal neural parenchyma, followed shortly thereafter (5 days after infection) by adherence of monocytes to vascular endothelium with migration into tissue and morphologic transformation into activated macrophages, concomitant with necrosis of neural cells which progresses from 1 to 3 weeks after infection. Removal of debris overlaps with and is followed by astrogliosis, collagen deposition, and vascular changes. Finally, several months after infection, an increasing infiltration of plasma cells occurs, accompanied by gradual disappearance of virus from the neural parenchyma. These morphologic observations suggest that the acut immunopathology is cell-mediated whereas local antibody production may play an important role in clearance of virus from persistently infected tissue.
D000818:Animals; D000831:Animals, Newborn; D002526:Cerebellar Diseases / Q000209:etiology* / Q000473:pathology; D002531:Cerebellum / Q000648:ultrastructure*; D005455:Fluorescent Antibody Technique; D008216:Lymphocytic Choriomeningitis / Q000150:complications* / Q000473:pathology; D008854:Microscopy, Electron; D051381:Rats