Volume 12, Issue 1 (2026)
Pharm Biomed Res 2026, 12(1): 1-8 |
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Jafari-Sales A, Hosseini-Karkaj K, Pashazadeh M. Oncogenic Potential of John Cunningham Virus (JCV) in Human Infection and Cancer Development. Pharm Biomed Res 2026; 12 (1) :1-8
URL: http://pbr.mazums.ac.ir/article-1-690-en.html
URL: http://pbr.mazums.ac.ir/article-1-690-en.html
1- Department of Microbiology, Kaz.C., Islamic Azad University, Kazerun, Iran.
2- Infectious Diseases Research Center, TaMS.C., Islamic Azad University, Tabriz, Iran.
2- Infectious Diseases Research Center, TaMS.C., Islamic Azad University, Tabriz, Iran.
Abstract: (136 Views)
Background: The John Cunningham virus (JCV), a prevalent and asymptomatic virus, can cause neurological complications, such as progressive multifocal leukoencephalopathy (PML) in immunocompromised individuals. Cancer is the second leading cause of death globally, with 10-15% of human cancers linked to viral infections, making JCV a significant tumor-inducing virus.
Objectives: This study aimed to examine the biology of JCV, its infection mechanisms, and the pathways that may facilitate tumorigenesis.
Methods: This narrative review employed a systematic approach to literature retrieval. Searches were conducted across major electronic databases, including PubMed, Scopus, Web of Science, and Google Scholar, to identify relevant publications up to early 2025. The search scope included a wide range of study designs, such as original research, reviews, systematic reviews, meta-analyses, and case reports. The search strategy utilized a combination of the following key terms: “John Cunningham virus” OR “JCV”, “JC virus”, “oncogenesis” OR “oncogenic”, “cancer development”, “infection”, and “human neoplasms.”
Results: The findings indicate that JCV disrupts key cellular pathways, including p53 and retinoblastoma protein (pRB) pathways, and its genomic integration into host DNA suggests its oncogenic potential. Its mechanisms include alterations in cell cycle control and Wnt signaling, promotion of cell proliferation, and potential interaction with β-catenin, leading to various cancers.
Conclusion: A better understanding of virus-related carcinogenesis could provide new targets for developing viral therapies that address not only viral infections but also cancer.
Objectives: This study aimed to examine the biology of JCV, its infection mechanisms, and the pathways that may facilitate tumorigenesis.
Methods: This narrative review employed a systematic approach to literature retrieval. Searches were conducted across major electronic databases, including PubMed, Scopus, Web of Science, and Google Scholar, to identify relevant publications up to early 2025. The search scope included a wide range of study designs, such as original research, reviews, systematic reviews, meta-analyses, and case reports. The search strategy utilized a combination of the following key terms: “John Cunningham virus” OR “JCV”, “JC virus”, “oncogenesis” OR “oncogenic”, “cancer development”, “infection”, and “human neoplasms.”
Results: The findings indicate that JCV disrupts key cellular pathways, including p53 and retinoblastoma protein (pRB) pathways, and its genomic integration into host DNA suggests its oncogenic potential. Its mechanisms include alterations in cell cycle control and Wnt signaling, promotion of cell proliferation, and potential interaction with β-catenin, leading to various cancers.
Conclusion: A better understanding of virus-related carcinogenesis could provide new targets for developing viral therapies that address not only viral infections but also cancer.
Type of Study: Review article |
Subject:
Cellular and Molecular Biology
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