Work

Genetic and chemical correction of cystic fibrosis reduces airway susceptibility to SARS-CoV-2

Year: 2026

Type: article

Abstract: Using rigorously controlled iPSC-derived airway models, the study shows that CFTR-deficient cells are more vulnerable to SARS-CoV-2 and display stronger inflammation than syngeneic CFTR-corrected controls. The CFTR modulator ETI reduces viral injury and boosts antiviral pathways in both CF and non-CF cells. Even at baseline, CFTR modulation enhances antiviral responses and lowers inflammation. Overall, the findings reveal a broad protective antiviral effect of CFTR modulators and highlight their therapeutic promise in inflammatory lung disease.

Source: American Journal of Physiology-Lung Cellular and Molecular Physiology

DOI: 10.1152/ajplung.00223.2025

Authors: Stuart D. Rollins, Adam J. Hume, Da-Yuan Chen, Ruth-Love Yeboah, Pushpinder Singh Bawa, Chantelle Simone-Roach, Jianing Yin, Alice Little, Anam Fatima, Hiroaki Murano, Luciana P. Tavares, Kenichi Okuda, Jessie Huang, Darrell N. Kotton, Mohsan Saeed, Elke Mühlberger, Ruobing Wang

Institutions: Boston Children's Hospital, Harvard University, Boston University, Boston Medical Center, University of North Carolina at Chapel Hill, Brigham and Women's Hospital, University of Southern California

Language: English

Topic: Cystic Fibrosis Research Advances

Subfield: Pulmonary and Respiratory Medicine

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green

Funders: Cystic Fibrosis Foundation, American Lung Association, Cystic Fibrosis Research, Massachusetts Consortium on Pathogen Readiness, National Heart, Lung, and Blood Institute

Awards: G1174325391, G234226948, G372985576, G5348336110, G5372302043, G6206609134, G6326271676, Using Induced Pluripotent Stem Cells to Characterize Cystic Fibrosis, Integrated Training in Respiratory Research, Developing Pluripotent Stem Cells to Model and Treat Lung Disease, Derivation of lung epithelia from iPS cells for advanced disease modeling

OpenAlex ID: W7124882301

FWCI: 8.927

Cites: 79

Cited by: 2

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