The role of pioneering transcription factors, chromatin accessibility and epigenetic reprogramming in oncogenic viruses
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Updated: Sep 17, 2025

Author Spotlight: Reprogramming Cancer Cells to iPSCs to Study Disease Progression and Treatment Targets
Published on: February 2, 2024
Mankgopo Kgatle1,2,3, Saidon Mbambara1,2,4, Leon Khoza1,2
1Department of Nuclear Medicine, University of Pretoria and Steve Biko Academic Hospital, Pretoria, South Africa.
Abstract:
Oncogenic viruses typically manipulate host cellular mechanisms to drive tumorigenesis. They exploit pioneering transcription factors to modify gene expression, enabling uncontrolled proliferation. These viruses alter chromatin accessibility and induce chromatin remodelling, disrupting DNA repair and promoting viral genome integration. Additionally, epigenetic reprogramming through mechanisms like DNA methylation and histone modifications silences tumor suppressor genes and activates oncogenes. Understanding these mechanisms is critical for identifying more improved therapeutic targets, improving diagnostics, and predicting disease progression. Advances in this field can guide the development of innovative treatments and early detection tools. This comprehensive review synthesizes existing knowledge on the contributions of oncogenic viruses such as hepatitis B virus (HBV), hepatitis C virus (HCV), human papillomavirus (HPV), and human T-cell leukaemia virus type 1 (HTLV-1), Epstein-Barr virus (EBV), human herpesvirus 8 (HHV-8), and Merkel cell polyomavirus (MCV) to cancer development, highlighting their therapeutic relevance and driving forward research in viral oncogenesis.
Insights
Oncogenic viruses drive cancer by altering host gene expression and DNA repair. Understanding these viral oncogenesis mechanisms is key for developing new cancer therapies and diagnostics.
Area of Science:
- Oncology
- Virology
- Molecular Biology
- Epigenetics
Background:
- Oncogenic viruses manipulate host cellular machinery to promote cancer development.
- These viruses utilize transcription factors, alter chromatin accessibility, and induce epigenetic reprogramming.
- Key viruses implicated include HBV, HCV, HPV, HTLV-1, EBV, HHV-8, and MCV.
Purpose of the Study:
- To comprehensively review the mechanisms by which oncogenic viruses contribute to cancer.
- To highlight the therapeutic relevance of understanding viral oncogenesis.
- To synthesize current knowledge and guide future research in viral oncology.
Main Methods:
- Literature review and synthesis of existing research on viral oncogenesis.
- Analysis of molecular and epigenetic mechanisms employed by oncogenic viruses.
- Examination of the roles of specific viruses (HBV, HCV, HPV, HTLV-1, EBV, HHV-8, MCV) in tumorigenesis.
Main Results:
- Oncogenic viruses exploit host transcription factors to drive uncontrolled proliferation.
- Viral activity leads to altered chromatin accessibility, impaired DNA repair, and genome integration.
- Epigenetic reprogramming, including DNA methylation and histone modification, silences tumor suppressors and activates oncogenes.
Conclusions:
- Understanding viral oncogenic mechanisms is crucial for developing targeted therapies and diagnostics.
- Advances in this field can lead to innovative treatments and early cancer detection tools.
- This review provides a foundation for further research into viral contributions to cancer.
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