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Updated: Sep 29, 2025
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Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
Published on: March 8, 2012
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Human papillomavirus type 16 E6 induces cell competition
Nicole Brimer1, Scott Vande Pol1
1Department of Pathology, University of Virginia, Charlottesville, Virginia, United States of America.
Plos Pathogens
|March 23, 2022
Summary
High-risk human papillomavirus (HPV) E6 protein drives cell competition, enabling infected cells to displace normal cells. This finding reveals a new role for E6 in tumor development beyond traditional oncogenicity.
Area of Science:
- Oncology
- Virology
- Cell Biology
Background:
- High-risk human papillomavirus (HPV) infections are linked to squamous epithelial tumors.
- HPV-infected cells initially expand at the expense of uninfected cells, but the mechanisms are not fully understood.
Purpose of the Study:
- To investigate the role of specific HPV16 oncoproteins in cell competition.
- To elucidate the mechanism by which HPV-infected cells displace normal keratinocytes.
Main Methods:
- Developed an in vitro assay using HPV16-expressing keratinocytes and uninfected keratinocytes.
- Assessed the contribution of HPV16 E6, E5, and E7 oncoproteins to cell competition.
- Investigated the interaction between E6 and p53.
Main Results:
- HPV16 E6 expression alone, not E5 or E7, conferred enhanced colony competition.
- E6-expressing keratinocytes displaced adjacent normal keratinocytes by undermining their substrate contact.
- E6 interaction with p53 was required for this cell competition.
Conclusions:
- HPV16 E6 oncoprotein is primarily responsible for cell competition, distinct from E7's role in oncogenicity.
- This study identifies a novel biological function for high-risk HPV E6 oncoproteins in promoting tumor development through cell competition.
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