The role of infection in asthma is presently a paradox. While respiratory syncytial virus, among others, has long been believed to instigate immunological changes which lead to asthma, and rhinovirus might be an important contributory factor in the exacerbation of asthma symptoms in children and adults, there is increasing speculation that infections in early life have a protective role in the development of allergy and asthma. The motivation for this theory was the observation of a strong relationship between birth order and the risk of allergic disease and generic atopy which has consistently emerged from British cohorts spanning the last 40 years.1-3 One of the appeals of the infection hypothesis is its undoubted capacity to explain the increase in allergic disease in developed societies over recent years as an inevitable consequence of improved hygiene standards, increased immunisation, and reduced contact between children owing to declining family size and less crowded homes. A theory which was once based exclusively on epidemiological associations has now gained support on immunological grounds. As the mechanisms which control the immune response to allergen and the course of the events in early life leading to maturation of this system become better understood, it is evident that the microbial environment of early life is a potential influence on this process.4 Neither epidemiology nor immunology yet provide much evidence on the nature of the infection or infections likely to be involved, but each supplies some useful, though sometimes disparate, clues.

In this issue of Thorax Farooqi and Hopkin have taken a retrospective look at all the available health records of a relatively recent (1975–1984) birth group taken from a single general practice in Oxfordshire, and examined links between a diversity of early childhood infections and the subsequent diagnosis of allergic disease.5 This historical cohort study …