It is widely accepted that T helper type 1 (T_H1) cytokines such as interferon-γ (IFN-γ) antagonize allergic diseases mediated by T_H2 cytokines. The 'hygiene hypothesis' has also proposed that decreased childhood exposure to pathogen-derived T_H1 cytokines may underlie the recent increased prevalence of asthma, a T_H2-mediated disease. We show here that influenza A viral infection, which induces large amounts of intrapulmonary IFN-γ production, unexpectedly enhanced later allergen-specific asthma and promoted dual allergen–specific T_H1 and T_H2 responses. Pulmonary dendritic cells obtained from the lung after viral clearance and resolution of acute inflammation conferred enhanced allergic disease and concurrent T_H1 and T_H2 immune responses, and these effects were dependent on IFN-γ secreted during the acute viral infection. Thus, respiratory viral infection and the acute T_H1 response can positively regulate T_H2-dependent allergic pulmonary disease in vivo, at least in part, by altering pulmonary dendritic cell function.