Stable Transformation of Mouse, Rabbit and Monkey Cells and Abortive Transformation of Human Cells by BK Virus, a Human Papovavirus

Portolani, Marinella; Borgatti, M.; Corallini, Alfredo; Cassai, Enzo; Grossi, Maria Pia; Barbanti‐Brodano, Giuseppe; Possati, L

doi:10.1099/0022-1317-38-2-369

Cited by 40 publications

(24 citation statements)

References 10 publications

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“…Although human cells are permissive for BKV replication (Takemoto & MuUarkey, 1973), they have been transformed by BKV. In addition to abortive transformation of human foreskin and embryonic fibroblasts (Shah et al, 1976;Portolani et al, 1978), stable transformation of human embryonic kidney and foetal brain cells has been described (Purchio & Fareed, 1979;Takemoto et al, 1979). In these reports, however, transformation was always 0022-1317/82/0000-5245 $02.00 © 1982 SGM associated with persistent BKV infection and virus production.…”

Section: Introductionmentioning

confidence: 99%

Transformation of Human Embryonic Fibroblasts by BK Virus, BK Virus DNA and a Subgenomic BK Virus DNA Fragment

Grossi

Caputo

Meneguzzi

et al. 1982

Journal of General Virology

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SUMMARYHuman embryonic fibroblasts (HEF) have been transformed by BK virus (BKV) DNA and by u.v.-inactivated or live BKV alone or in association with methylcholanthrene (MTC). The transformed cells produced BKV large T and small t antigens as well as the cellular 53 kdal protein, detected by immunofluorescence and immunoprecipitation. After an initial phase of lysis and virus shedding, virus or its coat protein antigen could not be detected in transformed cells. All human transformed cell lines could be superinfected by BKV or BKV DNA, but their susceptibility to superinfection was 20-to 500-fold lower than normal HEF. BKV could be rescued by fusion of transformed cells with normal HEF or Veto cells and by transfection of normal HEF with total DNA and DNA extracted from the Hirt supernatant of transformed cells. Blot hybridization analysis of DNA from transformed cells showed a considerable amount of free BKV DNA in monomeric and polymeric forms. Integrated BKV DNA was absent in most cell lines but present in only small amounts in BKV-transformed cells treated with MTC. Analysis of free BKV DNA with various restriction endonucleases and by blot hybridization showed that monomeric forms were complete BKV genomes, whereas polymers contained both complete and defective or rearranged BKV DNA. Transformation of HEF was also obtained with a 3.7 kilobase (kb) fragment of the BKV genome, produced by sequential digestion of BKV with the restriction endonucleases HhaI and EcoRI. This fragment extends clockwise on the virus genome from 0 to 72-2 map units and contains the entire early region. Blot hybridization analysis of cells transformed by the HhaI/EcoRI 3.7 kb fragment showed two separate integrations of BKV sequences without free virus DNA.

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Section: Introductionmentioning

confidence: 99%

Transformation of Human Embryonic Fibroblasts by BK Virus, BK Virus DNA and a Subgenomic BK Virus DNA Fragment

Grossi

Caputo

Meneguzzi

et al. 1982

Journal of General Virology

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“…It resides in a subclinical persistent state in the urinary tracts of healthy individuals and reactivates in immunosuppressed transplant patients, in whom it is associated with hemorrhagic cystitis and polyomavirus nephropathy (5,35,57,68). BKV transforms rodent cells in culture (64), causes kidney tumors in transgenic mice (15), and immortalizes primary human cells alone (32,65,77,82) or in the presence of other oncogenes such as c-ras (59) and adenovirus E1A (90). A possible role for BKV in human cancers is controversial because such a high percentage of the human population is exposed to the virus at a very early age, precluding the use of epidemiologic methods to test an association (16).…”

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BK Virus as a Cofactor in the Etiology of Prostate Cancer in Its Early Stages

Das

Wojno²,

Imperiale

2008

J Virol

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Prostate cancer has been projected to cause almost 10% of all male cancer deaths in the United States in 2007. The incidence of mutations in the tumor suppressor genes Rb1 and p53, especially in the early stages of the disease, is low compared to those for other cancers. This has led to the hypothesis that a human virus such as BK virus (BKV), which establishes a persistent subclinical infection in the urinary tract and encodes oncoproteins that interfere with these tumor suppressor pathways, is involved. Previously, we detected BKV DNA in the epithelial cells of benign and proliferative inflammatory atrophy ducts of cancerous prostate specimens. In the present report, we demonstrate that BKV is present at a much lower frequency in noncancerous prostates. Additionally, in normal prostates, T-antigen (TAg) expression is observed only in specimens harboring proliferative inflammatory atrophy and prostatic intraepithelial neoplasia. We further demonstrate that the p53 gene from atrophic cells expressing TAg is wild type, whereas tumor cells expressing detectable nuclear p53 contain a mix of wild-type and mutant p53 genes, suggesting that TAg may inactivate p53 in the atrophic cells. Our results point toward a role for BKV in early prostate cancer progression.

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“…BKV transforms rodent, monkey and human cells (Portolani et al, 1975(Portolani et al, , 1978Purchio & Fareed, 1979;Takemoto et al, 1979;Grossi et al, 1982) and is oncogenic in hamsters, mice and rats. Tumours induced in experimental animals include brain tumours, tumours of pancreatic islets, osteosarcomas and fibrosarcomas (Corallini et al, 1977Costa et al, 1976;Uchida et al, 1976Uchida et al, , 1979.…”

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confidence: 99%

Characterization of BK virus variants rescued from human tumours and tumour cell lines

Negrini

Rimessi²,

Mantovani³

et al. 1990

Journal of General Virology

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Stable Transformation of Mouse, Rabbit and Monkey Cells and Abortive Transformation of Human Cells by BK Virus, a Human Papovavirus

Cited by 40 publications

References 10 publications

Transformation of Human Embryonic Fibroblasts by BK Virus, BK Virus DNA and a Subgenomic BK Virus DNA Fragment

Transformation of Human Embryonic Fibroblasts by BK Virus, BK Virus DNA and a Subgenomic BK Virus DNA Fragment

BK Virus as a Cofactor in the Etiology of Prostate Cancer in Its Early Stages

Characterization of BK virus variants rescued from human tumours and tumour cell lines

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