This study uncovers mutations in BKPyV genome affecting oncogenesis in tumor-derived rodent cell lines, suggesting significant implications in virology.
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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Shioda et al. (2025) studied this question.
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