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Asthma is a common chronic disease of childhood, but for unknown reasons disease activity sometimes subsides as children mature. To understand why, we exposed mice across a range of ages to viral and allergic triggers of asthma exacerbations and airway pathology. We found that pathology induced by Sendai virus (SeV) or in uenza A virus (IAV) occurred selectively in juvenile mice in a microbiomeindependent manner, while the same phenotypes induced by allergens were insensitive to age. Age-speci c responses to SeV included a juvenile bias towards type-2 airway in ammation that emerged early in infection and was lost with maturation. With aging, we observed progressive transcriptional changes to alveolar macrophages (AMs) including the acquisition of high-level MHC-II expression. Importantly, depleting AMs canceled the protective effects of maturity on post-viral airway pathology. Thus, aging of the lung-immune microenvironment in uences chronic outcomes of respiratory viral infection and may help to explain childhood asthma remission.