Virus infections in infant mice causing persistent impairment of turnover of brain catecholamines.

Newborn mice were inoculated with attenuated Coxsackie type B4 virus. Three-to-4-day old mice were infected with yellow fever virus vaccine. A number of mice survived the acute infections. Some of these demonstrated residual neurological symptoms, some showed recovery from symptoms while others survived the infection without revealing symptoms of disease. Determinations of dopamine, noradrenaline, 5-hydroxytryptamine, homovanillic acid and 5-hydroxyindoleacetic acid in the inoculated brains indicated an imparied turnover of neurotransmitters. Subnormal concentrations of catecholamines and homovanillic acid were encountered in the acutely-infected mice as well as among the survivors. Failure to synthesize catecholamines was observed not only in mice demonstrating symptoms of disease or in animals which recovered from their infection but also among a proportion of the mice which never demonstrated neurological symptoms. In contrast, 6-week-old Swiss albino mice infected with West Nile virus showed no effect on the turnover of brain monoamines either in acutely infected mice or in animals which survived the acute infection. Herpes simplex virus infection of 3-week-old mice induced during the acute infection an increased release of neurotransmitters. When these mice were "cured" of the infection by increasing the environmental temperature the elevated turnover of monoamine metabolism was normalized. Two months later there were no differences in concentrations of catecholamines or homovanillic acid between infected animals or uninfected controls. Thus, persistent impairment of brain monoamine metabolism was induced in mice infected when very young. The possible importance of the observations, in particular the findings of an impaired turnover after subclinical infection, is discussed.