Role of parainfluenza virus-specific IgE in pathogenesis of croup and wheezing subsequent to infection.

In order to determine the role of parainfluenza virus-specific IgE antibody production and release of histamine in the pathogenesis of lower respiratory disease caused by parainfluenza virus infection, we studied 84 infants and children at the time of parainfluenza virus infection. Parainfluenza virus-IgE antibody was detected in samples of nasopharyngeal secretions by means of an enzyme-linked immunosorbent assay, and histamine content of nasopharyngeal secretions was determined by a fluorometric technique. Virus-specific IgE responses appeared earlier and were of greater magnitude in patients with croup, wheezing, and croup with wheezing caused by parainfluenza virus infection than in patients with parainfluenza virus-induced upper respiratory illness. Histamine was detectable in nasopharyngeal secretions of patients with parainfluenza virus-related croup significantly more often than in patients with upper respiratory illness caused by parainfluenza virus. These observations suggest a role for immunologic mechanisms in the pathogenesis of severe forms of respiratory illness caused by parainfluenza virus infection.

Natural history of parainfluenza virus infection in childhood.

In order to determine the natural history of parainfluenza virus infection in early life, we followed prospectively 130 infants and children from birth or a few months of age for evidence of infection with PV. Using rapid diagnostic techniques, standard tissue culture infectivity, and serologic techniques we were able to document primary PV infection in 92% of these infants, and repeated infection with heterotypic or homotypic PV strains in 49% by 30 months of age. Increasing patient age had no significant effect in reducing the incidence of lower respiratory tract illness as a result of PV infection. Infection with one PV serotype provided no protection against LRTI at the time of subsequent infection with a heterotypic PV strain. In contrast, primary PV infection provided a brief period of immunity to LRTI upon homotypic reinfection. Secretory IgA responses to PV were determined by immunofluorescent techniques. Antibody response to PV strains causing primary infection and heterotypic repeated infection were transient and of low magnitude. Homotypic reinfection resulted in significantly enhanced production of secretory antibody to PV. At least in early life, repeated exposures to PV appear to be essential for maintaining immunity to severe forms of illness caused by PV infection.