Intrauterine infection of mice with St. Louis encephalitis virus: immunological, physiological, neurological, and behavioral effects on progeny.

Intravenous injection of pregnant mice with St. Louis encephalitis (SLE) virus at 8 days of gestation resulted in infection of the fetus. Progeny developed no antibody or tolerance to SLE virus since the viral antigen was cleared by maternal antibody before antibody-forming competence developed in the young. Temporary growth retardation was observed in a number of young at 3 weeks of age. After the initial setback the growth rate increased, indicating that early runting was due to an inability to adjust adequately to extrauterine life, which was subsequently overcome. In most other young there were no significant effects on growth, reproduction, or life expectancy. A few young died at or shortly after birth; in these, neurological changes ranging from gross defects such as encephaloceles and hydrocephalus to histological evidence of necrosis and congestion were observed. Neurologically related behavioral changes were detected by using the open field test and the rotating-rod test, which indicated neurological damage and memory impairment in the surviving intrauterinely infected animals.