Pneumovirus-induced bronchiolitis causes ~200,000 deaths per year in developing nations and is a risk factor for subsequent asthma in the developed world. Bronchiolitis is characterised by airway epithelial cell (AEC) death and sloughing, neutrophilic inflammation, alarmin release and elevated viral burden. We have previously established that the absence of interferon regulatory factor 7 (IRF7), a critical regulator of antiviral immunity, increases susceptibility to Pneumovirus-associated bronchiolitis and subsequent asthma in mice. Here we address whether necroptotic cell death is active in acute viral infection, and whether inhibition of necroptosis-associated proteins, receptor-interacting protein kinase-1 (RIP1K) and mixed lineage kinase domain-like protein (MLKL), ameliorates bronchiolitis and later asthma. Pneumovirus infection significantly up-regulated RIPK1 and MLKL expression, at both the gene and protein level in IRF7-deficient, but not WT mice. Of note, the two kinases co-localised at the apical surface of airway epithelial cells at 8 to 10 days post infection (dpi), coinciding with epithelial cell sloughing, alarmin release and neutrophilic inflammation. Genetic or pharmacological inhibition of phosphorylated RIP1K and MLKL significantly decreased RIPK1/MLKL expression, alarmin release, neutrophil infiltration, and epithelial cell sloughing. Inhibition of necroptosis in early-life prevented development of airway hyperreactivity and airway remodelling, hallmark features of asthma, following viral challenge in later-life. Pneumovirus infection of human bronchial epithelial cells induced necroptosis, as evidenced by the phosphorylation of RIP1K and MLKL, which contributed to subsequent translocation of alarmins. Together, these data suggest that inhibition of necroptosis may be a viable strategy to limit viral bronchiolitis and break its nexus with asthma.