Pathogenesis of cerebellar hypoplasia produced by lymphocytic choriomeningitis virus infection of neonatal rats. 1. Evolution of disease following infection at 4 days of age.

Intracerebral inoculation of 4-day-old rats with lymphocytic choriomeningitis virus (E-350 strain) produced a nonfatal, acute, severe, and permanent cerebellar necrosis with minimal histological evidence of inflammation. Virus persisted in the brain at high titers for 30 to 40 days and was finally cleared about 120 days after infection. Rabbit anti-rat lymphoid serum prevented cerebellar necrosis, and brain virus titers were higher than in control animals receiving normal rabbit serum. Thus, the immune response which clearly is responsible for the cerebellar lesion also plays a role in the gradual suppression of infection.