Affiliations: Pediatric Intensive Care Unit, Hospital Sant Joan de Deu, University of Barcelona, Barcelona, Spain
Note: [] Corresponding author: I. Jordan Garcia, Pg. Sant Joan de Deu n˚ 2, 08950, Esplugues de Llobregat, Barcelona, Spain. Tel.: +34 932 532 158; Fax: +34 932 033 959; E-mail: [email protected].
Abstract: Respiratory syncytial virus (RSV) is among the primary pathogens of bronchiolitis. The mortality rate among hospitalized children with RSV bronchiolitis is approximately 1 to 3%. As reported by various authors, the severity of this viral disease is linked to immune response. Thus, it is important that treatment for RSV bronchiolitis be immunologically targeted. The virus activates intracellular signaling in respiratory epithelial cells via receptors known as Toll-like receptors. After this stimulation, primary RSV infection generates a mixed Th1/Th2 response, which is regulated by gamma interferon. An exacerbated Th2 response would lead to a more severe infection. Herein we review the immunologic mechanisms behind RSV bronchiolitis in order to correlate each treatment with a corresponding immunological response.
