RHINOVIRUSES IN SEATTLE FAMILIES, 1975–1979

Rhinovirus infections in Seattle families with schoolchildren (1975–1979) and in selected outpatients were revealed by virus shedding or antibody rise. These observations extend those in the Seattle Virus Watch (1965–1969). Analysis of rhinovirus serotype prevalence again revealed certain “common” persisting serotypes but provided no further evidence that new serotypes are continuing to emerge. Two seasonal peaks, spring higher than fall, were again evident infection rates, again inversely related to age, were lower overall than in the Virus Watch (0.42 vs. 0.64 per person-year), probably because there were fewer young children. Frequencies of antibody response by virus shedders again varied widely by serotype but differed greatly from those in the Virus Watch in rank order of response rate, suggesting that immunogenicity is not a stable serotype characteristic. The frequency and magnitude of antibody response of virus shedders increased with age. Antibody-related protection against infection was evident only in persons age ≥10 years. Observations in 7 families during successive homotypic infection episodes indicate that postinfection immunity to natural challenge requires persistence of antibody. Of all reported respiratory illnesses, 11.9% (0.31 per person-year) were due to rhinoviruses and 6.9% to influenzavi-ruses. Of viruses recovered from family members, rhinoviruses, herpes simplex, and influenza comprised 56%, 12.6%, and 12.4%, respectively. Although households often experienced ≥2 concurrent or closely consecutive episodes of infection with different viruses, only 29 individuals were shown to shed 2 viruses at the same time. Most of the second viruses, including 3 rhinoviruses and 18 other nonhemadsorbing viruses, appeared when 582 rhinovirus-positive specimens were retested after treatment with homotypic antibody. These results suggest that rhinoviruses interfere with nonhemadsorbing viruses in cell culture but mostly with other rhinoviruses in humans.