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Related Experiment Videos

The papillomavirus life cycle.

John Doorbar1

  • 1Division of Virology, National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK. jdoorba@nimr.mrc.ac.uk

Journal of Clinical Virology : the Official Publication of the Pan American Society for Clinical Virology
|March 9, 2005
PubMed
Summary

Papillomaviruses require epithelial differentiation for their life cycle, with gene expression tightly regulated during cell migration. High-risk human papillomaviruses (HPVs) can cause abortive infections, potentially leading to cancer.

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Area of Science:

  • Virology
  • Cell Biology
  • Oncology

Background:

  • Papillomaviruses infect epithelial cells, relying on differentiation for life cycle completion.
  • Viral gene expression is regulated as infected cells migrate and differentiate within the epithelium.

Purpose of the Study:

  • To elucidate the regulated expression of papillomavirus genes during the epithelial life cycle.
  • To understand the factors influencing viral genome replication and virion production.
  • To explore the outcomes of papillomavirus infections, including abortive infections and their link to cancer.

Main Methods:

  • Analysis of viral gene product expression patterns in different epithelial layers.
  • Investigation of the conditions required for viral genome amplification and virion assembly.

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  • Comparative analysis of papillomavirus life cycles across related viruses and hosts.

    • Main Results:

    • E6 and E7 expression in basal layers promote S-phase and proliferation, facilitating viral genome replication.
    • Genome amplification is triggered by increased replication proteins and co-expression of specific viral proteins.
    • Capsid protein expression occurs in upper epithelial layers, coinciding with E4 expression.

    Conclusions:

    • Papillomavirus life cycle progression is tightly linked to epithelial differentiation and regulated gene expression.
    • Variations in viral proteins and host interactions influence the success of viral replication and disease outcome.
    • Abortive papillomavirus infections, particularly with high-risk HPVs, can act as a predisposing factor for cancer development.