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In this issue

Our first three papers are investigating various aspects of respiratory syncytial virus (RSV) infection. Many previous publications have discussed associations between RSV bronchiolitis and subsequent atopy and asthma. The topic remains contentious (1, 2). Here we have a paper from Korea highlighting age-related differences in responses to the virus, a subject that has been addressed in a previous paper (3). In this study infants over 12 months of age infected with RSV were more capable of generating interferon gamma than those below 6 months of age. This is likely to account for the greater severity of disease in the younger age group. Furthermore, low interferon gamma generation in response to the infection has in the past has been associated with atopy, although in this study atopy was an exclusion criterion (4). We have also previously published information on the release of cysteinyl leukotrienes in RSV infection in a murine model (5). In this issue we have measurements of the leukotrienes in human infants during RSV bronchiolitis compared with healthy controls showing significantly raised levels in nasal lavage fluid but this was independent of the family history of atopy or exposure to tobacco smoke. It begs the question as to whether leukotriene receptor antagonist drugs might have a role in the management of this condition. However, the paper from Finland suggests that there is no subsequent increase in consumption of asthma medicines amongst infants who have been exposed to an RSV epidemic under the age of 6 months. Conventional teaching suggests that it is only virus infections that aggravate wheezing. However, bacteria are isolated from wheezing infants quite frequently as shown in the study from Japan. It remains to be established whether this is merely colonization or actual infection contributing to the pathology. However, as has been shown previously, allergic children are more prone to severe respiratory infections than those who are non-allergic and maybe there is a common underlying immune deviation contributing both to atopic wheezing and bacterial infection (6). Identification of risk factors for the development of asthma, allergy and both has been a focus for a vast number of publications in the journal and recently there have been some innovative suggestions such as a relationship between vitamin D intake and allergy (7). However, the relationship with antenatal and postnatal environmental tobacco smoke exposure is certainly not new with papers published over several decades. The prevailing opinion is that exposure antenatally and/or postnatally is not associated with an increased risk of allergy (8). We now have an excellent paper from Perth, Australia emphasizing that maternal smoking while increasing respiratory problems in infancy does not have any impact on allergy. The study showed no effect of the smoking on mucosal immunity as evidenced by generation of immunoglobulin A (IgA). Thus the explanation for the increased frequency of respiratory illnesses lies elsewhere and may well be an impact of antenatal smoking on airway structure. Exposure antenatally to paracetamol has been another recent focus and we have a paper from Singapore employing a case–control study which points to paracetamol as increasing the risk of both allergic and non-allergic wheezing in early life. This supports the original observations of Shaheen et al. (9). The International Study for Asthma and Allergies in Childhood (ISAAC) has been going for many years and the questionnaires have become standard tools in epidemiological investigations. However it is important to be aware that at present they have only been validated for use in children and adolescents. A Scandinavian study has shown that while answers to the questionnaires are relatively reliable in identifying clinically diagnosed asthma in children above 2 yr of age, the sensitivity of the questionnaires is extremely low in 1to 2-yr olds. Alternative tools will be required. A Brazilian study has utilized the questionnaire to elaborate on adolescent asthma. Interestingly this has shown associations with the mother being a smoker, being the first child in the family and being exposed to Pediatr Allergy Immunol 2007: 18: 92–93