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Rous Sarcoma Virus (RSV) and Cancer01:03

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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
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Related Experiment Video

Updated: Aug 5, 2025

Induction and Analysis of Epithelial to Mesenchymal Transition
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Published on: August 27, 2013

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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.

Biorxiv : the Preprint Server for Biology
|March 30, 2023
PubMed
Summary
This summary is machine-generated.

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.

Keywords:
A549 cellsALI cultureE-cadherinNHBE cellsTGF-βcytoskeletonepithelial-mesenchymal transition (EMT)respiratory epitheliumrespiratory syncytial virus (RSV)vimentin

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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.