DNA viruses in human cancer: established oncogenic mechanisms, emerging virus–tumour associations and clinical implications
4 affiliations
- 1Department of Orthopedic Surgery, the Affiliated Hospital of Qingdao University, Qingdao, China
- 2Department of Gynecology, The Women and Children’s Hospital of Qingdao, Qingdao, China
- 3Department of Pediatrics, Peking University Third Hospital, Beijing, China
- 4Department of Ophthalmology, the Affiliated Hospital of Qingdao University, Qingdao, China
Abstract
DNA virus-associated tumours represent an important component of the global burden of infection-associated cancer. Studies of classical DNA tumour viruses have defined major oncogenic routes, including persistent viral oncoprotein expression, chronic inflammation and tissue regeneration, viral integration and immune evasion. This work has also facilitated clinical applications of vaccines, antiviral therapies and viral biomarker testing. Recent advances in cancer genomics and molecular pathology have identified several biologically distinctive virus–tumour associations. These include TTMV::RARA fusion-driven APL-like acute myeloid leukaemia, HPV42-associated digital papillary adenocarcinoma, AAV2 insertions in a subset of hepatocellular carcinomas and transplant-associated BKPyV-positive urothelial carcinoma. The significance of these associations lies not in expanding the catalogue of tumour viruses, but in revealing distinct molecular events. These encompass virus–host fusion, tissue-specific viral oncogene expression, insertion-mediated cis activation and persistent T-antigen expression under immunosuppression. Here, we outline the principal mechanisms of classical DNA tumour viruses and compare the molecular basis, modes of tumour maintenance and potential clinical value of these recently recognised associations. We also discuss detection strategies, evidentiary boundaries and priorities for future research. Current evidence indicates that event-matched assays may support specialist ancillary diagnosis or molecular classification in selected settings, particularly for APL-like leukaemia and DPA. However, none of the four emerging associations currently supports population screening or a virus-directed standard therapy, and research-stage applications require prospective validation.
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BibTeX
@article{liu2026viruses,
title = {{DNA viruses in human cancer: established oncogenic mechanisms, emerging virus–tumour associations and clinical implications}},
author = {Zhen Liu and Yan Wang and Ran Liu and Yuan-He Wang and Peng-Yuan Su and Zhi-Chao Han and Shuo Yuan and Bin-Hai Yu and Cheng-Ye Che and Shao-Qi Tian},
journal = {Frontiers in Cellular and Infection Microbiology},
year = {2026},
month = oct,
doi = {10.3389/fcimb.2026.1970942},
url = {https://doi.org/10.3389/fcimb.2026.1970942},
note = {CC BY},
}
RIS
TY - JOUR
TI - DNA viruses in human cancer: established oncogenic mechanisms, emerging virus–tumour associations and clinical implications
AU - Zhen Liu
AU - Yan Wang
AU - Ran Liu
AU - Yuan-He Wang
AU - Peng-Yuan Su
AU - Zhi-Chao Han
AU - Shuo Yuan
AU - Bin-Hai Yu
AU - Cheng-Ye Che
AU - Shao-Qi Tian
PY - 2026
DA - 2026/10/26
JO - Frontiers in Cellular and Infection Microbiology
DO - 10.3389/fcimb.2026.1970942
UR - https://doi.org/10.3389/fcimb.2026.1970942
AB - DNA virus-associated tumours represent an important component of the global burden of infection-associated cancer. Studies of classical DNA tumour viruses have defined major oncogenic routes, including persistent viral oncoprotein expression, chronic inflammation and tissue regeneration, viral integration and immune evasion. This work has also facilitated clinical applications of vaccines, antiviral therapies and viral biomarker testing. Recent advances in cancer genomics and molecular pathology have identified several biologically distinctive virus–tumour associations. These include TTMV::RARA fusion-driven APL-like acute myeloid leukaemia, HPV42-associated digital papillary adenocarcinoma, AAV2 insertions in a subset of hepatocellular carcinomas and transplant-associated BKPyV-positive urothelial carcinoma. The significance of these associations lies not in expanding the catalogue of tumour viruses, but in revealing distinct molecular events. These encompass virus–host fusion, tissue-specific viral oncogene expression, insertion-mediated cis activation and persistent T-antigen expression under immunosuppression. Here, we outline the principal mechanisms of classical DNA tumour viruses and compare the molecular basis, modes of tumour maintenance and potential clinical value of these recently recognised associations. We also discuss detection strategies, evidentiary boundaries and priorities for future research. Current evidence indicates that event-matched assays may support specialist ancillary diagnosis or molecular classification in selected settings, particularly for APL-like leukaemia and DPA. However, none of the four emerging associations currently supports population screening or a virus-directed standard therapy, and research-stage applications require prospective validation.
SN - 2235-2988
ER -