BK virus infection of the human urinary tract

Shinohara, Toshiya; Cheng, Seng H.; Marshall, John; Fujita, Miri; Nagashima, Kazuo

doi:10.1002/jmv.1890410408

Cited by 80 publications

(50 citation statements)

References 22 publications

(7 reference statements)

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“…Paraffin sections were deparaffinized, followed by enzyme retrieval and incubation with mouse anti-BKV large Tag monoclonal antibody, as previously described. 28,29 Pankeratin Information on tumor grade and smoking was missing for 1 and 7 patients, respectively. staining was also conducted on sections from both tumor and normal bladder to demonstrate the presence of viable antigen.…”

Section: Immunohistochemistry For Bkv T-antigenmentioning

confidence: 99%

Lack of BK virus DNA sequences in most transitional‐cell carcinomas of the bladder

Rollison¹,

Sexton²,

Rodríguez³

et al. 2006

Intl Journal of Cancer

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BK virus (BKV), a common human polyomavirus infection latent in the kidneys, can reactivate with immunosuppression to cause renal disease. Some have suggested that BKV may contribute to the development of bladder cancer, and BKV sequences have been reported from bladder tumors. To further examine the role of BKV in human bladder cancer, a series of bladder tumors was investigated for BKV genomic sequences. Fresh‐frozen specimens from 76 transitional cell carcinoma tissues and 46 paired adjacent normal urothelial tissues archived at the H. Lee Moffitt Cancer Center were studied. All tissues were histopathologically reviewed. DNA extracted from the tissues was tested by quantitative real‐time polymerase chain reaction (QPCR) assays to detect BKV DNA sequences in the VP1 coding region. Amplification of ERV‐3 was conducted separately to quantify cell copy number. Conventional PCR targeting the BKV T‐antigen (T‐Ag) coding region and immunohistochemistry for BKV T‐Ag were also conducted on all tissues that tested positive for BKV by QPCR. Seventy‐three bladder tumors yielded ≥3,000 copies of ERV‐3, 4 (5.5%) of which tested positive for BKV with average copy numbers of 7.9, 15.8, 0.4 and 0.3 per 1,000 cells. Paired normal tissue was available for 2 of these BKV‐positive tumors, 1 of which was BKV‐positive (14.6 copies/1,000 cells). No other normal tissues were BKV‐positive by QPCR. The 6 BKV‐positive tissues by QPCR were also positive by conventional PCR, but all stained negative for BKV T‐Ag by immunohistochemistry. BKV is unlikely to be involved in the etiology of most bladder tumors. © 2006 Wiley‐Liss, Inc.

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Section: Immunohistochemistry For Bkv T-antigenmentioning

confidence: 99%

Lack of BK virus DNA sequences in most transitional‐cell carcinomas of the bladder

Rollison¹,

Sexton²,

Rodríguez³

et al. 2006

Intl Journal of Cancer

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“…Sequence analysis of the viral origin of replication discovered the presence of point mutations in one of the samples, defining it as a new strain of BKV, designated as URO1. It has been shown in cell culture that similar mutations impair the replication ability of the virus, leading to an increased transformation potential (Shinohara et al, 1993). Hence, it was speculated that mutant genomes impaired for replication might integrate into the host genome and eventually lead to cancer.…”

Section: Introductionmentioning

confidence: 99%

Detection and expression of human BK virus sequences in neoplastic prostate tissues

2004

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“…Both viruses establish persistent subclinical infections in the kidneys and peripheral blood in 85% of the population worldwide (10,36). The urotheliotropic nature of BKV is characterized by infection of the epithelial lining of the collective ducts, the transitional epithelial cells of the renal calyces, the parietal epithelium of the Bowman's capsule, and the transitional epithelium of the renal pelvis and the urinary tract (11,56). Sporadic reactivation of BKV resulting in limited viral replication is seen in 0.5 to 20% of healthy seropositive individuals, yet renal function is left unaffected (20,23,62).…”

mentioning

confidence: 99%

Infection of Vero Cells by BK Virus Is Dependent on Caveolae

Eash

Querbes

Atwood

2004

J Virol

133

145

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Polyomavirus-associated nephropathy occurs in ϳ5% of renal transplant recipients and results in loss of graft function in 50 to 70% of these patients. The disease is caused by reactivation of the common human polyomavirus BK (BKV) in the transplanted kidney. The early events in productive BKV infection are unknown. In this report, we focus on elucidating the mechanisms of BKV internalization in its target cell. Our data reveal that BKV entry into permissive Vero cells is slow, is independent of clathrin-coated-pit assembly, is dependent on an intact caveolin-1 scaffolding domain, is sensitive to tyrosine kinase inhibition, and requires cholesterol. BKV colocalizes with the caveola-mediated endocytic marker cholera toxin subunit B but not with the clathrin-dependent endocytic marker transferrin. In addition, BKV infectious entry is sensitive to elevation in intracellular pH. These findings indicate that BKV entry into Vero cells occurs by caveola-mediated endocytosis involving a pH-dependent step.Humans are the natural host species for two members of the polyomavirus family, BK virus (BKV) and JC virus (JCV) (22). Both viruses establish persistent subclinical infections in the kidneys and peripheral blood in 85% of the population worldwide (10, 36). The urotheliotropic nature of BKV is characterized by infection of the epithelial lining of the collective ducts, the transitional epithelial cells of the renal calyces, the parietal epithelium of the Bowman's capsule, and the transitional epithelium of the renal pelvis and the urinary tract (11, 56). Sporadic reactivation of BKV resulting in limited viral replication is seen in 0.5 to 20% of healthy seropositive individuals, yet renal function is left unaffected (20,23,62). A dramatic increase in viral activity leading to disease progression occurs predominantly in the context of greatly impaired T-cell-mediated immunity (26,27).Kidney transplant recipients are subjected to a potent immunosuppressive therapy and are thus at a high risk for exacerbated BKV replication (1). Active BKV infection in the renal allograft, known as polyomavirus nephropathy, has been linked to progressive graft dysfunction and ultimate graft loss (13). Sustained high levels of viral replication result in lytic destruction of the host tubular cells and release of BKV progeny to perpetuate the infection (1, 33, 34). BKV, the causative agent of polyomavirus nephropathy, is drawing increasing attention as a significant factor in the failure of renal transplants (48).Similar to those of the other polyomaviruses, BK virions are small (40.5 to 45 nm in diameter) and consist of a superhelical circular double-stranded DNA genome contained within a nonenveloped icosahedral capsid (18). Though the exact identity of the BK receptor(s) is unknown, evidence suggests that gangliosides type II, GD1a, and GT play important roles in the initial interaction between BKV and the permissive monkey kidney (Vero) cell line, as well as in BKV hemagglutination of human type O red blood cells (54,59,60). Following pen...

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BK virus infection of the human urinary tract

Cited by 80 publications

References 22 publications

Lack of BK virus DNA sequences in most transitional‐cell carcinomas of the bladder

Lack of BK virus DNA sequences in most transitional‐cell carcinomas of the bladder

Detection and expression of human BK virus sequences in neoplastic prostate tissues

Infection of Vero Cells by BK Virus Is Dependent on Caveolae

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