Viral infections, especially those caused by rhinovirus, are the most common cause of asthma exacerbations. Previous studies have argued that impaired innate anti-viral immunity and, as a consequence, more severe infections contribute to these exacerbations.
These studies explored the innate immune response in the upper airway of allergic rhinitis and asthmatic volunteers in comparison to healthy controls and interrogated how these differences corresponded to severity of infection.
Allergic rhinitic, asthmatic, and healthy volunteers were inoculated with rhinovirus A16 and monitored for clinical symptoms. Tissue and nasal wash samples were evaluated for anti-viral signature and viral load.
Both allergic rhinitic and asthmatic subjects demonstrated more severe cold symptoms. Asthmatic subjects demonstrated worsened asthma control and increased bronchial hyperreactivity in the setting of higher exhaled breath FeNO and blood eosinophils. These studies confirmed reduced expression of interferons and virus-specific pattern recognition receptors in both atopic cohorts. However, despite this defect in innate immunity, allergic rhinitis/asthmatic volunteers demonstrated reduced rhinovirus concentrations in comparison to controls.
These results confirm that the presence of an allergic inflammatory disorder of the airway is associated with reduced innate immune responsive to RV infection. Despite this, these allergic volunteers demonstrate reduced viral loads, arguing for the presence of a compensatory mechanism to clear the infection.

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