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ABSTRACT: In order to determine whether IgE production occurs predominantly at mucosal or systemic sites, we studied the production of respiratory syncytial virus (RSV)- specific antibody in serum and nasopharyngeal secretions (NPS) from 41 patients with RSV infection using an enzyme- linked immunosorbent assay. RSV-IgE was found in higher titer in samples of NPS than in simultaneously obtained serum specimens at all phases of illness. Despite the excess dilution incurred in the collection process, RSVIgE was frequently detected in NPS specimens while it was undetectable in serum. In 20 selected subjects, ratios of RSV antibody in NPSrserum were 2.00 for RSV-IgE, 2.42 for RSV-IgA, and 0.01 for RSV-IgG. Also the geometric mean value of ratios of RSV-IgE:RSV-IgG was 1.74 in NPS and 0.05 in serum, while the geometric mean value of ratios of RSV-IgA:RSV-IgG were 1.85 in NPS and 0.09 in serum. These data suggest that IgE production occurs predominantly at mucosal surfaces.

ABSTRACT: Samples of nasopharyngeal secretions from a group of 73 infants with bronchiolitis or upper respiratory illness alone during infection with respiratory syncytial virus were analyzed for leukotriene C4(LTC4) content using a reverse-phase high-pressure liquid chromatography assay with confirmation by radioimmunoassay. Titers of respiratory syncytial virus (RSV)-specific IgE in nasopharyngeal secretion (NPS) specimens were determined using an enzyme-linked immunosorbent assay. The highest concentrations of LTC4were found in the first 3 to 8 days after the onset of illness, and LTC4was detectable in progressively lower concentrations in samples obtained up to 28 days after the onset of illness. LTC4was detected in samples of NPS obtained in the acute phase of illness from 67% of infants with bronchiolitis due to RSV and in 33% of samples of NPS obtained during the same interval from infants with upper respiratory illness alone (p < 0.025). Concentrations of LTC4in children with bronchiolitis were 5-fold higher (1271 pg/ml) then the mean concentration of LTC4in children with upper respiratory illness (224 pg/ml, p < 0.02). LTC4was detected in 83% of the children developing an RSV-IgE response and in 24% of subjects not developing an RSV-IgE response (p < 0.001). Quantities of LTC4measured in NPS were directly correlated with the magnitude of the RSV-IgE response in secretions (r = 0.33, p < 0.02). These studies lend support to previous investigations suggesting that severe bronchiolitis due to RSV results from IgE-mediated hypersensitivity reactions to viral antigens, with release of chemical mediators of airway obstruction. Their implications should be considered in new approaches to therapy of RSV bronchiolitis.

ABSTRACT. The relationship between the development of cytotoxic cellular immune response to herpes simplex virus type I (HSV-1)-infected autologous cells and the production of interferon (IFN) was studied using in vitro secondary sensitization of peripheral blood leukocytes in subjects with recurrent herpes labialis (RHL) and in normal controls without any history of recurrent herpes labialis. There was a significant discordance between optimal HSV-1 antigen dose required for induction of peak cytotoxic responses and for maximal activity of IFN. Moderate IFN activity (6–100 U/ml) was demonstrated in all HSV-1 antigen-stimulated peripheral blood leukocytes collected from subjects during both acute and convalescent phase of RHL. However, only 50% of seropositive controls and no seronegative controls exhibited detectable IFN activity, when stimulated with HSV-1 antigen, although such in vitro stimulation resulted in maximal virus-specific cell-mediated cytotoxicity. A correlation of virus specific cytotoxic activity to HSV-1 and IFN production (r = 0.38, p < 0.05) was less marked than that of cytotoxic activity to K562 (natural killer-sensitive target cells) and IFN titer (r = 0.48, p < 0.01). Furthermore significant reverse correlations between cytotoxicity against HSV-1-infected autologous cells and a titer of ?-IFN was observed in samples with high cytotoxic activity. These observations suggest that ?-IFN produced by HSV immune T cell may also act as an autoregulatory factor against the production of cytotoxic cellular activity against HSV-1-infected autologous cells.