During the past two decades, a large number of studies have addressed the association of viral respiratory events in early life and the subsequent development of recurrent wheezing and asthma later in life. 1e4 Investigations performed both in animal models and in humans have provided new insights into potential pathogenetic mechanisms discernible during acute and convalescent stages of viral events and their potential association with the long-term consequences of these events. 5 6 Retrospective analysis of clinical trials has suggested that the use of antirespiratory syncytial virus (RSV) antibodies may decrease the incidence of subsequent asthma-like symptoms, 7 but prospective data are lacking. The strongest data for the association between early RSV events and asthma comes from longitudinal studies. The Tucson Children’s Respiratory Study was based on a healthy and representative population, and its results, if not automatically applicable to all communities given the peculiarities of the Arizona desert, have been replicated in other population-based studies. The main findings from the Tucson study indicated that RSV, independent of other known risk factors for asthma, was significantly associated with recurrent wheeze in the first decade of life. 1 The results of a larger birth cohort, also population based, the ALSPAC study from Bristol points in the same direction as the Tucson study: children with a RSV bronchiolitis admission in the first year of life were more likely to have asthma at age 7years, compared with controls and there was no relation with RSV infection and the development of atopy at this age. 8 The issue of a possible relation between early life RSV bronchiolitis and the later development of atopy has been entertained by a series of studies, and the disparities of findings seem to be related to the methodology used in selecting the subjects. A major strength of these two abovementioned birth cohort studies is that they are population based, and are powered adequately enough to study asthma and atopy as main outcomes, in a scenario in which a great number of other independent risk factors were also ascertained. Valuable information comes from a subset of children in the Tucson study who had infant lung function testing before any viral event was detected; these children were more likely to wheeze with lower respiratory illnesses if they had lower lung function values as measured by maximal expiratory flow at functional residual capacity [V! maxFRC]. 9 Infant lung function data were not evaluated in relation to severe bronchiolitis or RSV bronchiolitis in the Tucson study, but this was done in birth cohort from Perth, in which 253 healthy infants were followed from birth and had lung function measured at 1, 6 and 12 months of life. Similarly to the Tucson findings, infants in Perth who had bronchiolitis were in the lowest quartile for premorbid lung function values. 10 When this cohort was re-evaluated years later, children with bronchiolitis were shown to be at an increased risk of wheezing and, more interestingly, their expiratory flows at age 11 years were significantly lower compared with the rest of the cohort, and these levels tracked with the lower expiratory flows observed in the first months of life. 11 These findings indicate that premorbid lung function predicts low lung function that may not (at least not significantly) be affected by the acute viral bronchiolitis event.

In this issue of Thorax, Sigurs and collaborators12 (see page 1045) offer new insights into mechanisms relating early life severe viral bronchiolitis and later asthma. These investigators revisit their cohort, for which almost 18years ago they originally enrolled two groups of …