Rhinovirus infection preferentially increases lower airway responsiveness in allergic subjects

Rhinovirus (RV) infections are important triggers of acute asthma symptoms in susceptible persons. To determine whether the presence of allergy is a risk factor for enhanced lower airway effects during RV infection, we experimentally infected (RV16) 18 volunteers with allergic rhinitis and 13 normal control subjects and measured the effects on the response of the lower airways to histamine. All subjects were successfully infected, as indicated by increased upper respiratory symptoms and RV16 cultured from nasal secretions. The change in histamine PD₂₀(ΔPD₂₀) caused by RV infection was significantly different in allergic subjects from that in nonallergic control subjects (ΔPD₂₀ = -0.40 versus -0.03 log units, p = 0.04). This relationship was strengthened after adjusting for initial PD₂₀ and FEV₁ (mean ΔPD₂₀ = -0.43 versus 0.01 log units, p < 0.01). The virus-induced ΔPD₂₀ was also influenced by baseline lung function: there was a positive correlation between initial FEV₁ and ΔPD₂₀, and a weak but significant negative correlation between baseline PD₂₀ and ΔPD₂₀. These findings indicate that host factors such as allergy, baseline FEV₁, and baseline PD₂₀ influence the changes in lower airway physiology caused by RV infection and raise the possibility that these factors contribute to the increased lower airway effects of RV infection in subjects with asthma.