MINI REVIEW article
Front. Cell. Infect. Microbiol.
Sec. Virus and Host
Volume 15 - 2025 | doi: 10.3389/fcimb.2025.1617198
Oncogenic Viruses Rewire the Epigenome in Human Cancer
Provisionally accepted
- Cancer Research Group (CRG), Faculty of Medicine, Universidad de Las Américas, Quito, Ecuador
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Viruses contribute to approximately 15–20% of global cancer cases, yet the full spectrum of their oncogenic mechanisms continues to be uncovered. Beyond the classical roles of genome integration, chronic inflammation, and immune evasion, mounting evidence reveals that oncogenic viruses—including the human papillomavirus (HPV), Epstein–Barr virus (EBV), hepatitis B virus (HBV), hepatitis C virus (HCV), and Human T-cell leukemia virus type 1 (HTLV-1)—profoundly reshape the host epigenome to establish persistent infection and promote tumorigenesis. These viruses orchestrate widespread and durable changes in DNA methylation, histone modification, chromatin accessibility, and non-coding RNA expression, silencing tumor suppressors, deregulating oncogenic pathways, and inducing stemness-like phenotypes. In this review, we provide a comprehensive synthesis of how distinct oncogenic viruses modulate the epigenetic landscape across tissue contexts, with a focus on cervical, hepatic, and lymphoepithelial cancers. We also explore how these virus-induced epigenetic “scars” may persist after viral clearance and highlight recent advances in therapeutic targeting. Emerging therapeutic strategies that integrate oncolytic virotherapy, epigenetic drugs, and immune modulation through combinational therapy offer synergistic mechanisms to overcome immune resistance and epigenetic silencing in virus-induced cancers. These integrated approaches hold transformative potential for more durable and targeted treatment outcomes.
Keywords: Oncogenic virus, Oncolytic virotherapy, epigenome, Cancer, Immune Modulation, drugs
Received: 24 Apr 2025; Accepted: 19 May 2025.
Copyright: © 2025 Bautista and López-Cortés. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Andrés López-Cortés, Cancer Research Group (CRG), Faculty of Medicine, Universidad de Las Américas, Quito, Ecuador
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