【Abstract】 Objective To investigate the effects of respiratory syncytial virus ( RSV) infection on the dynamic changes of airway hyperresponsiveness ( AHR) in ovalbumin ( OVA) -induced asthma in mice.Methods 60 BALB/c female mice were randomly divided into PBS control group ( A group, n = 6) , OVA group, OVA/RSV group, dexamethasone group ( D group, n =6) . Kinetics of AHR of OVA group mice was carried out on day 21, 25, 29 and 33 ( B1, B2, B3, B4 groups, n =6) , and the same with the OVA /RSV group( C1, C2, C3, C4 groups, n = 6 ) . The mouse asthma model was established by OVA-sensitization of intraperitoneal injection and repeated inhalation of OVA while the mice in OVA/RSV group were treated with combined intranasal inoculation with RSV ( 1. 0 ×106 pfu/mL in 50 μL) . Airway resistance of expiringphase ( RL ) and compliance of throax and lung ( CTL ) with different doses of acetylcholine ( Ach) were measured. Lung tissue sections were stained with hematoxylin and eosin ( HE) and periodic acid-Schiff ( PAS) for general morphology. Results Compared with B1 group, RL increased and CTL decreased in C1 group when Ach dose is above 5 g/L ( P lt; 0. 05, respectively) , and the effects prolonged ( 6 d, 10 d after challenge with OVA, respectively) much more than B1 group ( 2 d after challenge with OVA) . Compared with C1 group, RL decreased and CTL increased in D group and the infiltration of inflammatory cells was obviously alleviated in C1 group after treatment with dexamethasone. Conclusions Airway hyperresponsiveness increases obviously in OVA-sensitized and RSV-infected mice. The prolonged increase inRL and decrease in CTL ( 6 d, 10 d, respectively) may imply that RSV infection aggravates airway inflammation. The small airway inflammation may play a critical role in the persistence of airway hyperresponsiveness.