title: Interferon-gamma levels in nasopharyngeal secretions of infants with respiratory syncytial virus and other respiratory viral infections.
abstract: Respiratory syncytial virus (RSV) infection, one of the most common causes of hospitalization of children in developed countries, has been implicated as a cause of asthma. We aimed to characterize the cytokine profile in nasopharyngeal aspirates (NPAs) taken from infants during upper respiratory tract infection to investigate whether RSV induced a unique immune response as compared with other viruses. Additionally, we sought to determine whether this profile was influenced by the infants' atopic status. A prospective birth cohort of babies at high risk of atopy was recruited. Ratios of a T-helper 1 (Th1) cytokine, interferon gamma (IFN-gamma) and a T-helper 2 (Th2)-like cytokine, interleukin-10 (IL-10), in NPAs were determined during episodes of respiratory tract infections in the first year. The viral aetiology of the respiratory tract infections was determined using polymerase chain reaction (PCR), culture and immunofluorescence. Atopic status was ascertained at 1 year of age using skin prick tests. Participants were recruited antenatally and subsequently followed in the community. Sixty babies with one or both parents atopic were enrolled into the study. IFN-gamma : IL-10 ratios in NPAs during upper respiratory tract infections and their correlation with viral aetiology and atopic status were the main outcome measures. The mean IFN-gamma : IL-10 ratio was significantly lower (due to lower IFN-gamma) during RSV infections than during infections with other viruses (P = 0.035). The cytokine ratio, however, did not differ between infants with or without wheeze during URTIs (P = 0.44), or between infants who were atopic or non-atopic (P = 0.49). This study suggests that RSV is associated with lower IFN-gamma production in young babies, regardless of their atopic status, compared to upper respiratory tract infections where either another virus is detected or where no viral identification is made.
authors.affiliation: Department of Immunology and Infectious Diseases, Royal Alexandra Hospital for Children, Westmead, NSW, Australia. PreetiJ@chw.edu.au
authors.forename: P
authors.initials: P
authors.lastname: Joshi
authors.forename: A
authors.initials: A
authors.lastname: Shaw
authors.forename: A
authors.initials: A
authors.lastname: Kakakios
authors.forename: D
authors.initials: D
authors.lastname: Isaacs
mesh_terms: D005500:Follow-Up Studies; D006801:Humans; D006967:Hypersensitivity / Q000175:diagnosis / Q000276:immunology; D007223:Infant; D007371:Interferon-gamma / Q000032:analysis*; D016753:Interleukin-10 / Q000032:analysis; D009305:Nasopharynx / Q000276:immunology*; D011446:Prospective Studies; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology*; D018113:Respiratory Syncytial Virus, Human; D012141:Respiratory Tract Infections / Q000276:immunology; D012306:Risk; D012882:Skin Tests; D018709:Statistics, Nonparametric
chemical_list: D016753:Interleukin-10; D007371:Interferon-gamma