Early-life respiratory infection has been associated with asthma in later-life. Particularly, early-life human rhinovirus (RV) infection has been linked to asthma development in high risk infants and children. Nevertheless, the role of RV infection in the initiation of asthma remains unclear. In Dr. Hong's doctoral research, RV infection in neonatal mice induces type 2 immune response, while infection in adult mice elicits type 1 immune response. Age-dependent induction of type 2 cytokines, such as IL-25, IL-33, and IL-33 leads to the increase of type 2 innate lymphoid cells (ILC2). Type 1 cytokine, IFN-γ, is able to reduce the function of ILC2 in type 2 immune response. Finally, neonatal RV infection provokes persistent mucous metaplasia and airway hyperresponsiveness, the asthma-phenotype, which is not observed in adulthood infection. These results suggest that early-life RV infection can contribute to the initiation of persistent asthma by provoking age-dependent type 2 immune response.