已发表论文

病毒致癌机制:人类癌症中的 DNA 和 RNA 病毒

 

Authors Yao N, Huang B

Received 19 March 2025

Accepted for publication 4 October 2025

Published 15 December 2025 Volume 2025:18 Pages 17611—17631

DOI https://doi.org/10.2147/JIR.S529301

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Professor Ning Quan

Nana Yao,1,2 Bo Huang1 

1Department of Pathology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, 110000 People’s Republic of China; 2Department of Pathology, The 7th People’s Hospital of Zhengzhou, Zhengzhou Cardiovascular Hospital, Henan, Zhengzhou, People’s Republic of China

Correspondence: Bo Huang, Department of Pathology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, No. 44 Xiaoheyan Road, Dandong District, Shenyang 110000, People’s Republic of China, Email huangbo@cancerhosp-ln-cmu.com

Abstract: With 13% of global tumorigenesis related to pathogens and 2.2 million new tumour cases related to viral infections every year, the role played by viruses in tumorigenesis cannot be ignored. At present, the viruses that have been identified as carcinogenic substances are EB virus, hepatitis B virus, hepatitis C virus, Kaposi’s sarcoma virus, human immunodeficiency virus type 1, human T-cell lymphotropic virus type 1, human papillomavirus, Merkel cell polyomavirus, and BK virus. There are also a number of viruses which have not been designated as carcinogens, but which are also closely related to the tumours’ development, such as Simian virus 40, JC virus and human cytomegalovirus. Human oncolytic viruses are divided into DNA oncolytic viruses and RNA oncolytic viruses, which are highly diverse and have different tumorigenic mechanisms. This article focuses on these confirmed DNA tumor viruses and RNA tumor viruses, delving into the various tumor types they cause and the mechanisms behind them. Based on the comparative analysis of their oncogenic pathways, we conclude that common mechanisms, such as the disruption of tumor suppressor proteins, chronic inflammation, and immune evasion, presenting actionable targets for both prophylactic intervention and precision therapy against virus-associated cancers.

Keywords: tumours, tumour virus, tumorigenic mechanism, SV40, mesothelioma