Evidence map›Paper›PMID 39197446›Full record

ArticleCell genomics2024

Rhinovirus infection of airway epithelial cells uncovers the non-ciliated subset as a likely driver of genetic risk to childhood-onset asthma.

Sarah Djeddi, Daniela Fernandez-Salinas, George X Huang, Vitor R C Aguiar, Chitrasen Mohanty, Christina Kendziorski, Steven Gazal, Joshua A Boyce, Carole Ober, James E Gern and 2 more

Abstract read
In one paragraph

Article in Cell genomics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Unique nasal cell states induced by common pediatric respiratory viruses.bioRxiv : the preprint server for biology · 2026
    Article
  6. Article
  7. Multi-omics to study chronic respiratory diseases and viral infections.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Sarah DjeddiDivision of Immunology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Daniela Fernandez-SalinasDivision of Immunology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Licenciatura en Ciencias Genómicas, Instituto de Biotecnología, Universidad Nacional Autónoma de México (UNAM), Cuernavaca, Morelos 62210, México.
George X HuangDepartment of Medicine, Harvard Medical School, Boston, MA 02115, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA.
Vitor R C AguiarDivision of Immunology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Chitrasen MohantyDepartment of Biostatistics and Medical Informatics, University of Wisconsin-Madison, Madison, WI 53726, USA.
Christina KendziorskiDepartment of Biostatistics and Medical Informatics, University of Wisconsin-Madison, Madison, WI 53726, USA.
Steven GazalDepartment of Quantitative and Computational Biology, University of Southern California, Los Angeles, CA 90007, USA; Norris Comprehensive Cancer Center, Keck School of Medicine, University of Southern California, Los Angeles, CA 90007, USA.
Joshua A BoyceDepartment of Medicine, Harvard Medical School, Boston, MA 02115, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA.
Carole OberDepartment of Human Genetics, University of Chicago, Chicago, IL 60637, USA.
James E GernDepartment of Biostatistics and Medical Informatics, University of Wisconsin-Madison, Madison, WI 53726, USA; Departments of Pediatrics and Medicine, University of Wisconsin School of Medicine and Public Health, Madison, WI 53726, USA.
Nora A BarrettDepartment of Medicine, Harvard Medical School, Boston, MA 02115, USA; Jeff and Penny Vinik Center for Allergic Disease Research, Division of Rheumatology, Immunology, and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA.
Maria Gutierrez-ArcelusDivision of Immunology, Boston Children's Hospital, Boston, MA 02115, USA; Department of Pediatrics, Harvard Medical School, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: mgutierr@broadinstitute.org.

Funding

Therapeutic Control of Aspirin-Exacerbated Respiratory DiseaseU19AI095219 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Nora Amanda Barrett · 2011 to 2026
$29.1M
IMMUNOLOGIC BASIS OF RESISTANCE AND HYPERSENSITIVITYT32AI007306 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Nora Amanda Barrett, Joshua A Boyce · 1985 to 2026
$12.2M
Project-003U19AI162310 · NIAID · UNIVERSITY OF CHICAGO · PI Marcelo A. Nobrega, Carole Ober · 2021 to 2026
$10.6M
Joint Biology Consortium Resource-based CenterP30AR070253 · NIAMS · BRIGHAM AND WOMEN'S HOSPITAL · PI Peter A Nigrovic, Jeffrey Andrew Sparks · 2016 to 2026
$9.4M
Type 2 Inflammation and Remodeling Elicited Through an LTE4/OXGR1-dependent pathwayR01AI134989 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Nora Amanda Barrett · 2019 to 2026
$5.1M
Type 2 Mucosal Inflammation Elicited Through an LTE4/GPR99-Dependent PathwayR56AI134989 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI BARRETT, NORA AMANDA · 2018 to 2018
$247k
NIAID NIH HHS R01 AI134989NIAID NIH HHS R56 AI134989NIAID NIH HHS T32 AI007306NIAID NIH HHS U19 AI095219NIAID NIH HHS U19 AI162310NIAMS NIH HHS P30 AR070253
6 · The paper itself

Abstract

Asthma is a complex disease caused by genetic and environmental factors. Studies show that wheezing during rhinovirus infection correlates with childhood asthma development. Over 150 non-coding risk variants for asthma have been identified, many affecting gene regulation in T cells, but the effects of most risk variants remain unknown. We hypothesized that airway epithelial cells could also mediate genetic susceptibility to asthma given they are the first line of defense against respiratory viruses and allergens. We integrated genetic data with transcriptomics of airway epithelial cells subject to different stimuli. We demonstrate that rhinovirus infection significantly upregulates childhood-onset asthma-associated genes, particularly in non-ciliated cells. This enrichment is also observed with influenza infection but not with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or cytokine activation. Overall, our results suggest that rhinovirus infection is an environmental factor that interacts with genetic risk factors through non-ciliated airway epithelial cells to drive childhood-onset asthma.

Indexed as

AsthmaEpithelial CellsGenetic Predisposition to DiseasePicornaviridae InfectionsRhinovirusChildCOVID-19HumansInfluenza, HumanRisk FactorsSARS-CoV-2airway epithelial cellsasthmagene by environmentgenome-wide association studygenomicsrhinovirustranscriptomics

Identifiers

PMID39197446
PMCPMC11480861

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.