Airway hyperresponsiveness is the most prominent functional abnormalit
y 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 facto
rs, virus infections appear to be clinically most relevant, since rece
nt epidemiological studies have shown that most asthma exacerbations i
n children are associated with positive nasopharyngeal viral identific
ation. The pathogenesis of virus-induced airway hyperresponsiveness ha
s been investigated by experimental virus infections in animals and in
man. Intranasal inoculation and/or inhalation of live attenuated infl
uenza virus, or certain strains of rhinovirus, have been shown to indu
ce 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 mech
anisms of virus-induced airway hyperresponsiveness are still unclear,
but may, in part, be similar to those involved in the pathogenesis of
asthma. Currently investigated hypotheses include: epithelial damage o
r dysfunction, immunological responses, inflammatory mediator release,
cholinergic and/or noncholinergic reflexes, and impaired beta-adrenoc
eptor function. Careful experimental studies, using modern laboratory
techniques, are needed to unravel the role of viruses in the developme
nt of airway hyperresponsiveness. The results of such studies can pote
ntially lead to an improvement of future asthma management