Shioda Setsuko, Kasai Fumio, Ozawa Midori, Ohtani Azusa, Iemura Masashi, Watanabe Ken, Kohara Arihiro
National Institute of Biomedical Innovation, Health and Nutrition, Ibaraki, Osaka, Japan.
Cell Engineering Division, BioResource Research Center, Tsukuba, Japan.
Microbiologyopen. 2025 Oct;14(5):e70061. doi: 10.1002/mbo3.70061.
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.
在本研究中，我们分析了源自三种啮齿动物细胞系的BK多瘤病毒（BKPyV）基因组，这些细胞系是通过将BKPyV注射到新生啮齿动物体内由实验诱导的肿瘤建立的。三种细胞系（Vn - 324、In - 1024和Vn1919）最近已保藏于JCRB细胞库（日本生物资源研究细胞库）。Vn - 324是由BKPyV Gardner株野生型501（wt - 501）诱导的仓鼠脉络丛乳头状瘤建立的。据报道，该细胞系使用间接免疫荧光法检测大T抗原呈阴性。在本研究中，我们使用逆转录聚合酶链反应（RT-PCR）检测了大T抗原的表达。In - 1024细胞是由仓鼠胰岛素瘤建立的。诱导其产生的BKPyV毒株尚未见报道。Vn1919是由噬斑形态突变体522（pm - 522）诱导的小鼠室管膜瘤建立的。源自Vn - 324基因组DNA和wt - 501的BKPyV的非编码控制区（NCCR）具有相同结构，而源自Vn1919基因组DNA和pm - 522的BKPyV的NCCR具有相同结构。但源自In - 1024的NCCR是独特的。我们发现源自In - 1024基因组DNA的BKPyV在病毒蛋白1、2和3（VP1、VP2和VP3）编码区有大片段缺失。这种变异体可能是一种增殖缺陷型突变体，它与其他突变体在人胚肾细胞中得以扩增。这些发现为NCCR突变在病毒致癌过程中的作用提供了见解。
