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Characterisation of cyclin D1 down-regulation in coronavirus infected cells

Sally M Harrison1, Brian K Dove, Lisa Rothwell

  • 1Institute of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK.

FEBS Letters
|March 16, 2007
PubMed

Insights

Infectious bronchitis virus (IBV) reduces cyclin D1 levels post-transcriptionally, causing cell cycle arrest. This viral mechanism targets cyclin D1 for degradation, independent of cell cycle stage.

Area of Science:

  • Virology
  • Molecular Biology
  • Cell Biology

Background:

  • Infectious bronchitis virus (IBV) is a positive-strand RNA coronavirus.
  • Viruses can manipulate host cell cycle regulation for replication.
  • Cyclin D1 is a key regulator of the G1/S phase transition.

Purpose of the Study:

  • To investigate the effect of IBV infection on cyclin D1 expression.
  • To determine the mechanism of cyclin D1 regulation by IBV.
  • To compare IBV's interaction with cyclin D1 to other coronaviruses.

Main Methods:

  • Quantitative real-time RT-PCR to measure cyclin D1 mRNA levels.
  • Western blot analysis to assess cyclin D1 protein levels.
  • Confocal microscopy to visualize cyclin D1 localization and changes.
  • Inhibition studies to probe viral-mediated degradation pathways.

Main Results:

  • IBV infection induced a G2/M phase cell cycle arrest.
  • Cyclin D1 levels were reduced post-transcriptionally in IBV-infected cells.
  • Cyclin D1 degradation was mediated by a virus-induced pathway, irrespective of cell cycle stage.
  • The IBV nucleocapsid protein did not interact with cyclin D1, unlike in SARS-coronavirus.

Conclusions:

  • IBV actively manipulates host cell cycle machinery by reducing cyclin D1.
  • A viral pathway targets cyclin D1 for degradation, contributing to cell cycle arrest.
  • IBV employs distinct mechanisms for host cell cycle manipulation compared to SARS-coronavirus.

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