Objective To explore the role of respiratory syncytial virus (RSV) infection in aggravating airway inflammation and airway resistance in murine asthma model. Methods A total of 30 6-8-week-old male BALB/c mice were equally divided into three groups randomly: the control group, ovalbumin (OVA) group (asthma group), and respiratory syncytial virus (RSV)/OVA group (RSV+asthma group). In OVA group, murine asthma model was established using an OVA sensitization; in OSV/RSV group, mice were firstly sensitized by OVA and subsequently infected with RSV intranasally for three times to make acute viral infection asthma model; and in control group, the mice received equal volume of PBS treatment. Twenty-four hours after the last challenge, the airway resistance was evaluated by mouse ventilator (Buxco RC). Inflammatory cell infiltration was measured in bronchoalveolar lavage fluid (BALF). Pulmonary tissue samples were collected and stained with H-E, PAS or VG to observe inflammation of pulmonary tissues. Results Pulmonary tissue of mice in OVA group had inflammatory cell infiltration, airway mucus secretions were visible, and collagen was seen around the airway. Pulmonary tissue of mice in OVA/RSV group had significant inflammatory cell infiltration, alveolar stenosis, telangiectasia congestion, airway mucus secretions and collagen deposition. Lung function and the proportion of BALF eosinophils (EOS%) in OVA group and OVA/RSV group were significantly different from that of the control group (P<0.05,P<0.01). Airway resistance and the EOS% in OVA/RSV group were significantly different from those of the OVA group (P<0.05). Conclusion RSV infection can aggravate the airway inflammation and result in airway resistance in murine asthma model.