ABSTRACT
Results from recent epidemiological studies suggest that respiratory viruses play a role in the development and/or expression of asthma in genetically susceptible individuals (1-3). Due to a lack of ready extrapolation of results from animal models to humans and the inherent difficulties in studying naturally acquired colds in humans, several investigators have used human experimental provocation models to explore this relationship (4-19). The methodologies used in these models and results are summarized in Table 1.lnterestingly, but not surprisingly, different investigators have reported conflicting results (4-13). For example, in a number of studies, bronchial reactivity and the late-phase asthmatic responses were increased in subjects experimentally infected with either rhinovirus or influenza virus (4,5,8-14). In contrast, a few other studies failed to detect an effect of experimental infection with either of these viruses on the lower airways (6,7,15-19). Moreover, few, if any, of the viruses delivered in experimental settings has been reported to trigger acute asthma or alter routine spirometric parameters, even when the study population included subjects with allergic rhinitis and/ or asthma, and virus was cultured from the lower airways (4-19).
