K. Grunberg et al., Experimental rhinovirus 16 infection causes variable airway obstruction insubjects with atopic asthma, AM J R CRIT, 160(4), 1999, pp. 1375-1380
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.