Abstract
Airway hyperresponsiveness is the most prominent functional abnormality in asthma. Although its aetiology is still unclear, it is well-known that allergen exposure and virus infections can temporarily induce or aggravate airway hyperresponsiveness. Among these environmental factors, virus infections appear to be clinically most relevant, since recent epidemiological studies have shown that most asthma exacerbations in children are associated with positive nasopharyngeal viral identification. The pathogenesis of virus-induced airway hyperresponsiveness has been investigated by experimental virus infections in animals and in man. Intranasal inoculation and/or inhalation of live attenuated influenza virus, or certain strains of rhinovirus, have been shown to induce airway hyperresponsiveness to various bronchoconstrictor stimuli in man. This indicates that experimental virus-infection, like allergen challenge, is an appropriate investigational model of asthma. The mechanisms of virus-induced airway hyperresponsiveness are still unclear, but may, in part, be similar to those involved in the pathogenesis of asthma. Currently investigated hypothesis include: epithelial damage or dysfunction, immunological responses, inflammatory mediator release, cholinergic and/or noncholinergic reflexes, and impaired beta-adrenoceptor function. Careful experimental studies, using modern laboratory techniques, are needed to unravel the role of viruses in the development of airway hyperresponsiveness. The results of such studies can potentially lead to an improvement of future asthma management.
