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Respiratory syncytial virus (RSV) bronchiolitis is not only the leading cause of hospitalization in U.S. infants, but also a major risk factor for asthma development. While emerging evidence suggests clinical heterogeneity within RSV bronchiolitis, little is known about its biologically-distinct endotypes. Here, we integrated clinical, virus, airway microbiome (species-level), transcriptome, and metabolome data of 221 infants hospitalized with RSV bronchiolitis in a multicentre prospective cohort study. We identified four biologically- and clinically-meaningful endotypes: A) clinical classic microbiome  M. nonliquefaciens  inflammation IFN-intermediate , B) clinical atopic microbiome  S. pneumoniae / M. catarrhalis  inflammation IFN-high , C) clinical severe microbiome mixed inflammation IFN-low , and D) clinical non-atopic microbiome  M.catarrhalis  inflammation IL-6 . Particularly, compared with endotype A infants, endotype B infants—who are characterized by a high proportion of IgE sensitization and rhinovirus coinfection,  S. pneumoniae/M. catarrhalis  codominance, and high IFN-α and -γ response—had a significantly higher risk for developing asthma (9% vs. 38%; OR, 6.00: 95%CI, 2.08–21.9; P = 0.002). Our findings provide an evidence base for the early identification of high-risk children during a critical period of airway development.

Integrated omics endotyping of infants with respiratory syncytial virus bronchiolitis and risk of childhood asthma