Abstract
Purpose of the Study. The role of respiratory syncytial virus (RSV) in stimulating an immunoglobulin E (IgE) antibody response and enhancing the development of asthma remains controversial. The aim of this study was to measure IgE, immunoglobulin A (IgA), and immunoglobulin G (IgG) antibody responses to immunodominant RSV antigens in nasal washes and serum samples from infants with and without respiratory symptoms.Study Population. Forty infants aged 6 weeks to 2 years (20 with wheezing, 9 with rhinitis, and 11 without respiratory tract symptoms) were included in the investigation.Methods. The children were enrolled in an emergency department during the mid-winter months and seen again at follow-up when they were asymptomatic. Nasal washes were obtained by standard methods and were evaluated for RSV antigen. Moreover, determination of antibody isotypes (IgE, IgA, and IgG) to RSV antigens was performed in nasal washes and serum samples by using an enzyme-linked immunosorbent assay. In a subset of nasal washes, IgE to RSV was also evaluated by using a monoclonal anti-FcE antibody-based assay.Results. At enrollment, 15 patients with wheezing, 2 with rhinitis, and 1 control subject tested positive for RSV antigen. Thirteen patients with wheezing were <6 months old, and most (77%) were experiencing their first attack. Among the children with positive test results for RSV antigen, an increase in both nasal wash and serum IgA antibody to RSV-Fa and Ga was observed at the follow-up visit. There was no evidence for an IgE antibody response to either antigen.Conclusions. Both IgA and IgG antibodies to the immunodominant RSV-Fa and Ga antigens were readily detected in the nasal washes and serum samples from patients in this study. The investigators were unable to demonstrate specific IgE antibody to these antigens and concluded that the production of IgE as a manifestation of a Th2 lymphocyte response to RSV is unlikely.Reviewer’s Comments. There have been numerous investigations suggesting that RSV bronchiolitis may be a risk factor for recurrent wheezing and the development of asthma during childhood. In some cases, investigators have suggested that a possible mechanism for this association begins with the ability of RSV to stimulate IgE antibody production. The current publication by de Alarcon et al summarizes a well-designed, focused investigation that could not detect the presence of specific IgE antibody to immunodominant RSV antigens during or after an infection in infants with this common respiratory virus. Data from this investigation directly questions IgE antibody production as the primary mechanism of RSV-induced bronchiolitis and subsequent wheezing and should help spark continued interest and debate in this research area.
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