BACKGROUND: Patients with chronic rhinosinusitis (CRS) commonly experience aggravation of their symptoms after viral upper respiratory infection (URI). Rhinovirus (RV) is the most common URI-causing virus. However, there is a lack of a mouse model of RV infection and in vivo studies investigating the effect of RV infection on CRS. METHODS: A mouse model of chronic allergic rhinosinusitis (CARS) was established by sensitizing to ovalbumin (OVA) through intraperitoneal injection followed by nasal challenges with OVA for 5 weeks. Both control and CARS mice were euthanized at 48 hours after infection with minor group RV serotype 1B (RV1B). Sinonasal complex samples were evaluated histologically; and interleukin (IL)-6, macrophage inflammatory protein (MIP)-2, IL-13, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma were measured in the nasal lavage fluid. The RV1B-infected areas in control and CARS mice were identified using immunofluorescence. RESULTS: In the infected control mice group, RV1B increased secretory hyperplasia in the sinonasal mucosa and the production of proinflammatory cytokines including INF-gamma, MIP-2, and IL-13. Immunohistochemical analysis of nasal mucosa from RV1B-infected mice presented abundant RV1B staining, which was distributed between the epithelium and the lamina propria. In the CARS group, the RV1B-infected area per unit was significantly higher than that in control mice. However, RV1B infection neither increased the proinflammatory cytokine secretion nor worsened the histology significantly. CONCLUSION: We successfully established a mouse model of upper airway RV infection by nasal inoculation with RV1B. Although there was histologically-proven increased RV infection in the CARS model, the infection did not intensify sinonasal inflammation.