No Evidence of Human Polyomavirus 9, WU and KI DNA in Kidney and Urinary Bladder Tumour Tissue Samples

Csoma, Eszter; Bidiga, László; Méhes, Gábor; Gergely, Lajos

doi:10.1159/000445120

Cited by 10 publications

(10 citation statements)

References 64 publications

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“…Protocols for KIPyV and WUPyV qPCR and positive controls were the same as described previously [39]. Plasmid-containing KIPyV isolate Stockholm 60 and AP-p002 plasmid with the half-genome of WUPyV were kindly provided by Tobias Allander and David Wang.…”

Section: Methodsmentioning

confidence: 99%

“…Colombara et al [31, 32] found that previous infections with these polyomaviruses were not associated with lung cancer. The DNA prevalence of KIPyV and WUPyV was studied in different cancer types [9, 11-13, 33-39], but only KIPyV was detected in lung carcinomas [11] and in benign skin tumours [35]. To date, the DNA prevalence of MWPyV was examined and detected in tonsillar cancer [9], but it was not found in mucosal melanoma [33].…”

Section: Introductionmentioning

confidence: 99%

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Survey of KI, WU, MW, and STL Polyomavirus in Cancerous and Non-Cancerous Lung Tissues

et al. 2017

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Background/Aims: The pathogenesis of the human polyomavirus (PyV) KI, WU, MW, and STL has not been elucidated yet. Respiratory transmission is suggested, but the site of the replication, tissue, and cell tropism is not clarified. KIPyV and WUPyV DNA and/or antigen were detected in normal lung tissues previously by others. In fact, a KIPyV DNA sequence was found in lung cancer samples. Up to date, there is no publication about the DNA prevalence of MWPyV and STLPyV neither in normal nor in cancerous lung tissues. The aim of the present study was to examine the DNA prevalence of these polyomaviruses in cancerous and non-cancerous lung tissue samples, in order to study the possible site for viral replication and/or persistence, and the potential association of these viruses with lung carcinogenesis as well. Methods: 100 cancerous and 47 non-cancerous, formalin-fixed paraffin-embedded lung tissue samples were studied for KIPyV, WUPyV, MWPyV, and STLPyV by real-time PCR. Results and Conclusion: Neither of the viruses was found in samples from small-cell, non-small-cell (adenocarcinoma, squamous-cell carcinoma and large-cell neuroendocrine lung cancer), mixed-type and non-differentiated lung carcinoma, and non-cancerous lung tissues (from patients with pneumonia, emphysema and fibrosis).

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Survey of KI, WU, MW, and STL Polyomavirus in Cancerous and Non-Cancerous Lung Tissues

et al. 2017

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“…So far, whether BKPyV has a causal role in the development of cancer was controversial. Early studies detected the presence of BKPyV large T antigens in prostate-, bladder- and kidney tumors [ 6 – 8 ], but several researchers thought BKPyV was unlikely to be involved in the etiology of most renal and bladder tumors because they had failed to detect BKPyV DNA in the cancer samples [ 9 – 11 ].…”

Section: Introductionmentioning

confidence: 99%

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

Zeng

Sun

Bao

et al. 2020

Virol J

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Background Recent studies have confirmed the integration of the BK polyomavirus (BKPyV) gene into the cellular genome of urothelial carcinomas in transplant recipients, further confirming the correlation between BKPyV and urothelial carcinomas after transplantation. However, the role BKPyV infections play in the biological function of bladder cancer remains unclear. Methods We developed a BKPyV-infected bladder cancer cell model and a mice tumor model to discuss the role of BKPyV infections. Results Our research proves that BKPyV infections promote the proliferation, invasion and migration of bladder cancer cells, while the activation of β-catenin signaling pathway is one of its mediation mechanisms. Conclusions We first described BKPyV infection promotes the proliferation, invasion and migration of bladder cancer. We verified the role of β-catenin signaling pathway and Epithelial-Mesenchymal Transition effect in BKPyV-infected bladder cancer. These results provide meaningful information towards the diagnosis and treatment of clinical bladder cancer.

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“…In this study, we tested this hypothesis, although we are not aware of any documented complementarity/synergy between polyomaviruses, as for instance has been described between DNA viruses, such as hepatitis B and D virus . At the same time, this approach offered the possibility to confirm our previously reported HPyV9 viremia rates in KTx patients, which were not found in a number of other comparable studies . Since TSPyV belongs to the same genus as HPyV9 (alpha polyomavirus), and is also detected in kidney tissue and urine, we included this polyomavirus in the analysis as well.…”

Section: Introductionmentioning

confidence: 99%

“…18 At the same time, this approach offered the possibility to confirm our previously reported HPyV9 viremia rates in KTx patients, which were not found in a number of other comparable studies. 15,19 Since TSPyV belongs to the same genus as HPyV9 (alpha polyomavirus), and is also detected in kidney tissue and urine, we included this polyomavirus in the analysis as well.…”

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confidence: 99%

Impact of HPyV9 and TSPyV coinfection on the development of BK polyomavirus viremia and associated nephropathy after kidney transplantation

Rijn

Wunderink

Brouwer

et al. 2019

Journal of Medical Virology

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Background BK polyomavirus (BKPyV) persistently infects the urinary tract and causes viremia and nephropathy in kidney transplantation (KTx), recipients. In a previous study, we observed an increased incidence and load of BKPyV viremia in KTx patients coinfected with human polyomavirus 9 (HPyV9). Here we sought confirmation of this observation and explored whether novel HPyVs that have been detected in urine (HPyV9 and trichodysplasia spinulosa polyomavirus [TSPyV]) potentially aggravate BKPyV infection. Methods A well‐characterized cohort of 209 KTx donor‐recipient pairs was serologically and molecularly analyzed for HPyV9 and TSPyV coinfection. These data were correlated with the occurrence of BKPyV viremia and BKPyVAN in the recipients within a year after KTx. Results Seropositivity for HPyV9 (19%) and TSPyV (89%) was comparable between donors and recipients and did not correlate with BKPyV viremia and BKPyVAN that developed in 25% and 3% of the recipients, respectively. Two recipients developed TSPyV viremia and none HPyV9 viremia. Modification of the predictive effect of donor BKPyV seroreactivity on recipient BKPyV viremia by HPyV9 and TSPyV was not observed. Conclusions Our data provide no evidence for a promoting effect of HPyV9 and TSPyV on BKPyV infection and BKPyVAN in renal allograft patients. Therefore, we do not recommend including HPyV9 and TSPyV screening in KTx patients.

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No Evidence of Human Polyomavirus 9, WU and KI DNA in Kidney and Urinary Bladder Tumour Tissue Samples

Cited by 10 publications

References 64 publications

Survey of KI, WU, MW, and STL Polyomavirus in Cancerous and Non-Cancerous Lung Tissues

Survey of KI, WU, MW, and STL Polyomavirus in Cancerous and Non-Cancerous Lung Tissues

BK polyomavirus infection promotes growth and aggressiveness in bladder cancer

Impact of HPyV9 and TSPyV coinfection on the development of BK polyomavirus viremia and associated nephropathy after kidney transplantation

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