Here, we leverage primary BECs from children with and without asthma that were differentiated to an organotypic state at an air liquid interface to show that type 2 inflammation, as modeled by high IL-13 conditioning (23,24), may not affect viral load, but rather alters other subsequent anti-viral and inflammatory processes that are relevant to the pathogenesis of viral-triggered asthma exacerbation. The gene discussed is IL13; the disease is asthma.