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RSV bronchiolitis versus rhinovirus: Difference in nasal airway microRNA profiles and NFκB signaling

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Although rhinovirus infection is associated with increased risks of acute and chronic respiratory outcomes during childhood compared with respiratory syncytial virus (RSV), the underlying mechanisms remain unclear. We aimed to determine differences in nasal airway microRNA profiles and their downstream effects between infants with rhinovirus and RSV bronchiolitis.


As part of multicenter cohort study of infants hospitalized for bronchiolitis, we examined nasal samples obtained from 16 infants with rhinovirus and 16 infants with RSV. We tested nasal airway samples using microarrays to profile global microRNA expression and determine the predicted regulation of targeted transcripts. We also measured gene expression and cytokines for NFκB pathway components.


Between the virus groups, 386 microRNAs were differentially expressed (FDR<0.05). In infants with rhinovirus, the NFκB pathway was highly ranked as a predicted target for these differentially expressed microRNAs compared with RSV. Pathway analysis using measured mRNA expression data validated that rhinovirus infection had up-regulation of NFκB family (RelA and NFκB2) and down-regulation of inhibitor κB family. Infants with rhinovirus had higher levels of NFκB-induced type-2 cytokines (IL-10 and IL-13; FDR<0.01).


In infants with bronchiolitis, rhinovirus and RSV infections had different nasal airway microRNA profiles associated with NFκB signaling.

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Author information


  1. Department of Emergency Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA

    • Kohei Hasegawa
    •  & Carlos A Camargo
  2. Computational Biology Institute, George Washington University, Ashburn, VA

    • Marcos Pérez-Losada
  3. Department of Pediatrics, George Washington University School of Medicine and Health Sciences and the Division of Emergency Medicine, Children's National Health System, Washington, DC

    • Marcos Pérez-Losada
    • , Stephen J Teach
    •  & Robert J Freishtat
  4. CIBIO-InBIO, Universidade do Porto, Campus Agrário de Vairão, Vairão, Portugal

    • Marcos Pérez-Losada
  5. Center for Genetic Medicine Research, Children's National Health System, Washington, DC

    • Claire E Hoptay
    • , Samuel Epstein
    •  & Robert J Freishtat
  6. Department of Medicine, Boston Children's Hospital, Boston, MA

    • Jonathan M Mansbach
  7. Department of Molecular Virology and Microbiology and Pediatrics, Baylor College of Medicine, Houston, TX

    • Pedro A Piedra
  8. Department of Integrative Systems Biology, George Washington University School of Medicine and Health Sciences, Washington, DC

    • Robert J Freishtat
  9. Department of Pediatrics, George Washington University School of Medicine and Health Sciences, Washington,

    • Robert J Freishtat


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Corresponding author

Correspondence to Kohei Hasegawa.