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Updated: Jul 3, 2026
06:57
Chromogenic In Situ Hybridization as a Tool for HPV-Related Head and Neck Cancer Diagnosis
Published on: June 14, 2019
Viral interaction: a possible contributing factor in head and neck cancer progression
Michael P Underbrink1, Stephen L Hoskins, Anna M Pou
1Departments of Otolaryngology, University of Texas Medical Branch, Galveston, TX 77555, USA. mpunderb@utmb.edu
Acta Oto-Laryngologica
|July 9, 2008
Summary
Human herpesvirus-8 (HHV-8) may enhance human papillomavirus-16 (HPV-16) oncogenic activity. HHV-8’s ORF50 protein up-regulates HPV-16 E7 transcription, potentially driving cell cycle changes and malignant transformation.
Area of Science:
- Oncogenic viral interactions
- Molecular virology
- Cell cycle regulation
Background:
- High-risk human papillomavirus-16 (HPV-16) is linked to head and neck cancers.
- HPV-16 E6 and E7 oncoproteins disrupt cell cycle control.
- Herpesviruses may potentiate HPV-16's effects on cell transformation.
Purpose of the Study:
- To investigate if human herpesvirus-8 (HHV-8) ORF50/Rta protein interacts with HPV-16.
- To determine if ORF50 alters HPV-16 E6 and E7 transcription or translation.
Main Methods:
- Protein shift assays assessed ORF50 binding to HPV-16 DNA.
- Real-time PCR quantified E6 and E7 mRNA levels after ORF50 transfection.
- Immunofluorescent confocal microscopy measured E6 and E7 protein expression and localization.
Main Results:
- Potential binding sites for ORF50 within the HPV-16 genome were identified.
- Significant upregulation of HPV-16 E7 transcription was observed in cells expressing ORF50.
Conclusions:
- HHV-8 ORF50 protein can bind to HPV-16 DNA.
- HHV-8 may potentiate HPV-16's role in cell cycle dysregulation and malignant transformation by upregulating E7 transcription.
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