Experimental rhinovirus 16 infection causes variable airway obstruction insubjects with atopic asthma

Exacerbations of asthma are often associated with rhinovirus infections. Ho wever, it has not been investigated whether rhinovirus infection can induce variable airway obstruction in asthma. We examined the effect of experimen tal rhinovirus 16 (RV16) infection on daily home recordings of FEV1 in 27 s ubjects (nonsmoking, atopic, mildly asthmatic) who participated in a parall el placebo-controlled study. The subjects used a microspirometer to record FEV1 three times daily from 4 d before until 10 d after RV16 (n = 19) or pl acebo (n = 8) inoculation. In addition, symptoms of asthma and symptoms of common cold were scored. Airway hyperresponsiveness to histamine was measur ed 3 d before and on Days 4 and 11 after RV16/placebo administration. Home recordings of FEV1 decreased significantly after RV16 infection, reaching a minimum 2 d after inoculation (ANOVA, p less than or equal to 0.005), whic h was significantly different from placebo (p less than or equal to 0.004). In the RV16 group the lowest FEV1 (expressed as a percentage of personal b est) during Days 0-3 after infection (mean +/- SEM: 78.7 +/- 2.6% versus ba seline: 85.6 +/- 1.2%, p = 0.008) correlated significantly with the cold sc ore(r = -0.47, p = 0.04), asthma score (r = -0.47, p = 0.04), and with the decrease in airway hyperresponsiveness on Day 4 as compared with baseline ( r = 0.50, p = 0.03). We conclude that experimental RV16 infection augments variable air way obstruction in subjects with asthma. This favors a causati ve role for rhinovirus colds in asthma exacerbations, and is in keeping wit h rhinovirus-induced worsening of airway inflammation.