ABSTRACT
Viral respiratory tract infections have been epidemiologically associated with asthma in at least two major ways (Figure 15.1). First, during infancy, certain viruses have been implicated as potentially being responsible for the inception of the asthmatic phenotype. Second, in patients with established asthma, particularly children, viral upper respiratory tract infections play a significant role in producing acute exacerbations of airway obstruction that may result in frequent outpatient visits or in hospitalizations. The increased propensity for viral infections to produce lower airway symptoms in asthmatic individuals may be related, at least in part, to interactions among allergic sensitization, allergen exposure and viral infections that act as co-factors in the induction of acute episodes of airflow obstruction, and more prolonged physiological effects in the form of increased airway responsiveness that may change the airway threshold response to various environmental irritants or stimuli (e.g. exercise). This chapter highlights the latter associations by describing experiments performed in humans that have evaluated the interactions between the most common virus documented to induce asthma exacerbations, rhinovirus (RV), and aeroallergen exposure to ragweed in individuals sensitized to this pollen.1
