Abstract
The effects of RVIs on airway reactivity are multiple but do not necessarily include direct changes in the intrinsic contractile properties of airway smooth muscle. Rather, respiratory viruses influence bronchial smooth muscle function through a variety of other mechanisms: production of virus-specific IgE antibodies, epithelial injury, polymorphonuclear-dependent inflammation, and enhanced mediator release. Thus, a common pathway to airway hyperreactivity during respiratory viral illnesses is an overall enhancement of factors that cause or lead to inflammation. When the airways become the target of enhanced inflammation, bronchial reactivity and obstruction are accentuated. Although many questions remain to be answered, future studies to evaluate the biology of respiratory virus effects on mechanisms of allergic sensitization and airway responsiveness promise to provide a greater understanding of the pathogenesis of asthma.
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