Journal
VIRUSES-BASEL
Volume 12, Issue 10, Pages -Publisher
MDPI
DOI: 10.3390/v12101072
Keywords
polyomavirus; transcription; tropism; cis-acting regulatory elements; cell type-specific transcription factors; epigenetic modifications
Categories
Funding
- National Institutes of Health (NIH) [R01CA187718, R21AR074073, R21AI149761]
- NCI Cancer Center Support Grant (NCI) [P30 CA016520]
- Penn CFAR pilot award [P30 AI 045008]
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Polyomavirus infection is widespread in the human population. This family of viruses normally maintains latent infection within the host cell but can cause a range of human pathologies, especially in immunocompromised individuals. Among several known pathogenic human polyomaviruses, JC polyomavirus (JCPyV) has the potential to cause the demyelinating disease progressive multifocal leukoencephalopathy (PML); BK polyomavirus (BKPyV) can cause nephropathy in kidney transplant recipients, and Merkel cell polyomavirus (MCPyV) is associated with a highly aggressive form of skin cancer, Merkel cell carcinoma (MCC). While the mechanisms by which these viruses give rise to the relevant diseases are not well understood, it is clear that the control of gene expression in each polyomavirus plays an important role in determining the infectious tropism of the virus as well as their potential to promote disease progression. In this review, we discuss the mechanisms governing the transcriptional regulation of these pathogenic human polyomaviruses in addition to the best-studied simian vacuolating virus 40 (SV40). We highlight the roles of viral cis-acting DNA elements, encoded proteins and miRNAs that control the viral gene expression. We will also underline the cellular transcription factors and epigenetic modifications that regulate the gene expression of these viruses.
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