Human Polyomavirus BK Genome Analysis in BKPyV Induced Rodent Cell Lines
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Updated: Aug 3, 2026

Bacterial Artificial Chromosomes: A Functional Genomics Tool for the Study of Positive-strand RNA Viruses
Published on: December 29, 2015
Setsuko Shioda1, Fumio Kasai2, Midori Ozawa1
1National Institute of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan.
Abstract:
In this study, we analyzed the BK polyomavirus (BKPyV) genome derived from three rodent cell lines established from experimentally induced tumors by injecting BKPyV into newborn rodents. Three cell lines (Vn-324, In-1024, and Vn1919) were recently deposited in the JCRB Cell Bank (Japanese Collection of Research Bioresource Cell Bank). Vn-324 was established from a hamster choroid plexus papilloma induced by BKPyV Gardner strain wild-type 501 (wt-501). This cell line was reported to be negative for the large T-antigen using indirect immunofluorescence. In this study, we examined the large T-antigen expression using the reverse-transcriptase-polymerase chain reaction (RT-PCR). In-1024 cells were established from hamster insulinoma. The strain of BKPyV from which were induced has not been reported. Vn1919 was established from a mouse ependymoma induced by the plaque morphology mutant 522 (pm-522). The noncoding control region (NCCR) of BKPyV derived from Vn-324 genomic DNA and wt-501 had the same structure, whereas the NCCR of BKPyV derived Vn1919 genomic DNA and pm-522 had the same structure. But the NCCR derived In-1024 was unique. We revealed that BKPyV derived from In-1024 genomic DNA had a large deletion in the viral proteins 1, 2, and 3 (VP1,(VP1, VP2, and VP3) coding region. This variant may be a proliferation-defective mutant, which was expanded in human embryonic kidney cells with other mutants. These findings provide insights into the role of NCCR mutations in viral oncogenesis.
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