In mice, intranasal infection with RSV induced both the production of IL-33 and the expression of ST2, which was accompanied with a massive infiltration of ST2+CD45+ cells in the lungs, suggesting that during the early phase of RSV infection, IL-33 targeting of ST2 expressing cells may play a critical role for the development of RSV-induced airway inflammation. The gene discussed is IL33; the disease is inflammatory response.