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

Yoshihiko Raita (), Marcos Pérez-Losada, Robert J. Freishtat, Brennan Harmon, Jonathan M. Mansbach, Pedro A. Piedra, Zhaozhong Zhu, Carlos A. Camargo and Kohei Hasegawa
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Yoshihiko Raita: Massachusetts General Hospital, Harvard Medical School
Marcos Pérez-Losada: The George Washington University
Robert J. Freishtat: Center for Genetic Medicine Research, Children’s National Hospital
Brennan Harmon: Center for Genetic Medicine Research, Children’s National Hospital
Jonathan M. Mansbach: Harvard Medical School
Pedro A. Piedra: Baylor College of Medicine
Zhaozhong Zhu: Massachusetts General Hospital, Harvard Medical School
Carlos A. Camargo: Massachusetts General Hospital, Harvard Medical School
Kohei Hasegawa: Massachusetts General Hospital, Harvard Medical School

Nature Communications, 2021, vol. 12, issue 1, 1-13

Abstract: Abstract 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) clinicalclassicmicrobiomeM. nonliquefaciensinflammationIFN-intermediate, B) clinicalatopicmicrobiomeS. pneumoniae/M. catarrhalisinflammationIFN-high, C) clinicalseveremicrobiomemixedinflammationIFN-low, and D) clinicalnon-atopicmicrobiomeM.catarrhalisinflammationIL-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.

Date: 2021
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DOI: 10.1038/s41467-021-23859-6

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