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Respiratory syncytial virus matrix protein induces lung epithelial cell cycle arrest through a p53 dependent pathway

Tao Bian1, John D Gibbs, Claes Örvell

  • 1Laboratory of Respiratory Biology, National Institute of Environmental Human Science, Durham, North Carolina, United States of America.

Plos One
|June 5, 2012
PubMed

Insights

Respiratory syncytial virus (RSV) matrix protein (RSV-M) causes lung epithelial cells to arrest, enhancing viral replication. This cell cycle arrest is dependent on the p53 pathway, offering a target for antiviral strategies.

Area of Science:

  • Virology
  • Cell Biology
  • Molecular Biology

Background:

  • Respiratory syncytial virus (RSV) is a leading cause of viral respiratory infections in children.
  • Previous research indicated RSV infection triggers lung epithelial cell cycle arrest, promoting viral replication.

Purpose of the Study:

  • To elucidate the mechanism behind RSV-induced cell cycle arrest.
  • To investigate the role of the RSV-matrix (RSV-M) protein in this process.

Main Methods:

  • RSV-M protein was transfected into A549 and primary human bronchial epithelial (PHBE) cells.
  • Cell proliferation rates and cell cycle phases (G1, G2/M) were analyzed.
  • Expression levels of p53, p21, and phosphorylated retinoblastoma protein (Rb) were assessed.
  • Experiments were conducted in p53-deficient H1299 cells, with and without p53 cDNA reintroduction.

Main Results:

  • RSV-M protein transfection led to slower cell proliferation in both cell types.
  • RSV-M induced G1 phase arrest in A549 cells and G1/G2/M phase arrest in PHBE cells.
  • RSV-M expression increased p53 and p21 levels and decreased Rb phosphorylation.
  • Cell cycle arrest was dependent on p53; it was absent in p53-deficient cells but restored upon p53 reintroduction.

Conclusions:

  • RSV-M protein induces lung epithelial cell cycle arrest via a p53-dependent pathway.
  • This p53-mediated cell cycle arrest enhances RSV replication.
  • Targeting the RSV-M/p53 interaction could be a therapeutic strategy against RSV infections.

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