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The Role of the JC Virus in Central Nervous System Tumorigenesis

Center for Neurovirology, Department of Neuroscience, Lewis Katz School of Medicine at Temple University, 3500 N. Broad Street, Philadelphia, PA 19140, USA
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Int. J. Mol. Sci. 2020, 21(17), 6236; https://doi.org/10.3390/ijms21176236
Received: 19 June 2020 / Revised: 22 August 2020 / Accepted: 24 August 2020 / Published: 28 August 2020
(This article belongs to the Section Molecular Oncology)
Cancer is the second leading cause of mortality worldwide. The study of DNA tumor-inducing viruses and their oncoproteins as a causative agent in cancer initiation and tumor progression has greatly enhanced our understanding of cancer cell biology. The initiation of oncogenesis is a complex process. Specific gene mutations cause functional changes in the cell that ultimately result in the inability to regulate cell differentiation and proliferation effectively. The human neurotropic Polyomavirus JC (JCV) belongs to the family Polyomaviridae and it is the causative agent of progressive multifocal leukoencephalopathy (PML), which is a fatal neurodegenerative disease in an immunosuppressed state. Sero-epidemiological studies have indicated JCV infection is prevalent in the population (85%) and that initial infection usually occurs during childhood. The JC virus has small circular, double-stranded DNA that includes coding sequences for viral early and late proteins. Persistence of the virus in the brain and other tissues, as well as its potential to transform cells, has made it a subject of study for its role in brain tumor development. Earlier observation of malignant astrocytes and oligodendrocytes in PML, as well as glioblastoma formation in non-human primates inoculated with JCV, led to the hypothesis that JCV plays a role in central nervous system (CNS) tumorigenesis. Some studies have reported the presence of both JC viral DNA and its proteins in several primary brain tumor specimens. The discovery of new Polyomaviruses such as the Merkel cell Polyomavirus, which is associated with Merkel cell carcinomas in humans, ignited our interest in the role of the JC virus in CNS tumors. The current evidence known about JCV and its effects, which are sufficient to produce tumors in animal models, suggest it can be a causative factor in central nervous system tumorigenesis. However, there is no clear association between JCV presence in CNS and its ability to initiate CNS cancer and tumor formation in humans. In this review, we will discuss the correlation between JCV and tumorigenesis of CNS in animal models, and we will give an overview of the current evidence for the JC virus’s role in brain tumor formation. View Full-Text
Keywords: Polyomavirus JC; tumors of central nervous system; CY and Mad-4 NCCR-transgenic mice; p53 and pRB oncosuppressor; DNA damage response (DDR); Wnt pathway; insulin receptor substrate-1 IRS-1 signaling Polyomavirus JC; tumors of central nervous system; CY and Mad-4 NCCR-transgenic mice; p53 and pRB oncosuppressor; DNA damage response (DDR); Wnt pathway; insulin receptor substrate-1 IRS-1 signaling
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MDPI and ACS Style

Ahye, N.; Bellizzi, A.; May, D.; Wollebo, H.S. The Role of the JC Virus in Central Nervous System Tumorigenesis. Int. J. Mol. Sci. 2020, 21, 6236. https://doi.org/10.3390/ijms21176236

AMA Style

Ahye N, Bellizzi A, May D, Wollebo HS. The Role of the JC Virus in Central Nervous System Tumorigenesis. International Journal of Molecular Sciences. 2020; 21(17):6236. https://doi.org/10.3390/ijms21176236

Chicago/Turabian Style

Ahye, Nicholas, Anna Bellizzi, Dana May, and Hassen S. Wollebo 2020. "The Role of the JC Virus in Central Nervous System Tumorigenesis" International Journal of Molecular Sciences 21, no. 17: 6236. https://doi.org/10.3390/ijms21176236

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