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Updated: Aug 5, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
RSV infection does not induce EMT
Sattya N Talukdar1, Brett McGregor1, Jaspreet K Osan1
1Department of Biomedical Sciences, University of North Dakota School of Medicine & Health Sciences, Grand Forks, North Dakota, United States of America.
Abstract:
Respiratory syncytial virus (RSV) infection does not cause severe disease in most of us despite suffering from multiple RSV infections in our lives. However, infants, young children, older adults, and immunocompromised patients are unfortunately vulnerable to RSV-associated severe diseases. A recent study suggested that RSV infection causes cell expansion, resulting in bronchial wall thickening in vitro. Whether the virus-induced changes in the lung airway resemble epithelial-mesenchymal transition (EMT) is still unknown. Here, we report that RSV does not induce EMT in three different in vitro lung models: the epithelial A549 cell line, primary normal human bronchial epithelial cells, and pseudostratified airway epithelium. We found that RSV increases the cell surface area and perimeter in the infected airway epithelium, which is distinct from the effects of a potent EMT inducer, TGF-β1-driven cell elongation-indicative of cell motility. A genome-wide transcriptome analysis revealed that both RSV and TGF-β1 have distinct modulation patterns of the transcriptome, which suggests that RSV-induced changes are distinct from EMT.
Insights
Respiratory syncytial virus (RSV) infection does not induce epithelial-mesenchymal transition (EMT) in lung models. RSV alters airway epithelium cell size, distinct from EMT-inducing factors.
Area of Science:
- Pulmonology
- Virology
- Cell Biology
Background:
- Respiratory syncytial virus (RSV) can cause severe respiratory illness, particularly in vulnerable populations.
- Previous research indicated RSV infection might cause bronchial wall thickening, prompting investigation into its cellular mechanisms.
- The potential link between RSV-induced lung changes and epithelial-mesenchymal transition (EMT) remained unclear.
Approach:
- Investigated RSV's effect on three distinct in vitro lung models: A549 cells, primary bronchial epithelial cells, and airway epithelium.
- Compared RSV-induced cellular changes with those caused by transforming growth factor-beta 1 (TGF-β1), a known EMT inducer.
- Conducted genome-wide transcriptome analysis to compare gene expression patterns between RSV infection and TGF-β1 treatment.
Key Points:
- RSV infection did not induce EMT in any of the tested in vitro lung models.
- RSV increased cell surface area and perimeter in infected airway epithelium, unlike TGF-β1-induced cell elongation.
- Transcriptome analysis revealed distinct gene modulation patterns for RSV and TGF-β1, differentiating RSV's effects from EMT.
Conclusions:
- RSV infection does not trigger EMT in the airway epithelium.
- RSV-induced cellular alterations in the lung airway are mechanistically distinct from EMT.
- Findings clarify the cellular response to RSV, differentiating it from EMT-associated processes.

