Respiratory syncytial virus in infants and children

Abstract

Respiratory syncytial virus (RSV) disease is a major cause of death and hospitalization in infancy and a frequent cause of morbidity throughout childhood. An epidemic occurred in the Washington, D. C. area in each of 16 respiratory disease seasons between 1957 and 1970. During the peak month of a “composite epidemic” 70% of bronchiolitis patients and 56% of all respiratory disease inpatients exhibited evidence of RSV infection. Approximately one-half of infants followed longitudinally were infected during their first RSV epidemic and almost all children were infected after living through two RSV epidemics. RSV infection does not produce solid resistance. First infection may have a 40% incidence of febrile pneumonitis; illness with reinfection is usually much less severe. Serum antibody does not protect as evident from the study of natural disease and the use of killed vaccine. Local antibody responses occur in natural illness. Possibly serum antibody in the absence of local antibody plays a part in illness. We have studied local and serum antibody response to potential attenuated vaccine: a 26°C-adapted RSV and a ts mutant RSV. Both produced the desired infection as evidenced by virus recovery, serum, and local antibody response. However, both appear to have had residual pathogenicity for young infants. This included mild bronchitis after the 26°C RSV and mild rhinitis, which might be acceptable, but also fever and otitis in one infant after the ts RSV. Also, some of the virus recovered in the ts studies had wild-type characteristics. An acceptable RSV vaccine strain will (a) infect without undergoing reversion or other genetic changes, (b) induce resistance to wild-type virus, (c) cause no or very mild inflammatory changes such as the rhinitis associated with the vaccines thus far tried.