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PubMed2006

Polyomavirus BK nephropathy: the effect of an early diagnosis on renal function or graft loss.

Polyomavirus BK nephropathy is a new complication among renal transplant patients. We studied 664 cadaver renal transplant recipients from February 1998 to February 2005, divided into two periods: 448 (group A, February 1998 to July 2003) and 176 (group B, August 2003 to February 2005). Twenty patients (3%) developed biopsy-confirmed polyomavirus BK nephropathy; 13 (2.9%) in group A after worsening renal function and 7 (3.9%) in group B after a prospective cytologic study in urine, examining for decoy cells, and a qualitative polymerase chain reaction (PCR) assay in urine and blood. The mean time to diagnosis was higher among group A (15.0 +/- 1.6 versus 7.2 +/- 4.0 months), as was the serum creatinine (2.5 +/- 0.7 versus 2.0 +/- 0.6 mg/dL). After 12 months the serum creatinine was 2.7 +/- 1.3 versus 1.7 +/- 0.2 mg/dL, respectively. Poor prognostic factors were a persistently positive PCR in blood and viral inclusions in the control biopsy.

Adult↗

PubMed1990

Rapid detection of polyomavirus BK by a shell vial cell culture assay.

Polyomavirus BK (BKV) causes asymptomatic latent infection in the human host that is reactivated during periods of immune suppression. Detection by conventional tube cell culture is difficult and time consuming because BKV exhibits slow growth with late (14 to 28 days) and subtle cytopathic effects. We developed a shell vial cell culture assay (SVA) using a cross-reactive monoclonal antibody to the T antigen of simian virus 40 to detect BKV rapidly by indirect immunofluorescence. Nuclear fluorescence was seen in BKV-infected cells as early as 16 h postinoculation; 6 to 28 times more foci were present at 36 h postinoculation. Human embryonic kidney cells infected with BKV produced 7 to 42 times more fluorescent foci than MRC-5 or rhabdomyosarcoma cells did. Centrifugation enhanced the infectivity of BKV in the SVA. To define the clinical utility of SVA, urine specimens from organ transplant patients were tested. Of 27 patients, 4 (15%) were found to be positive by SVA. SVA offers a simple and rapid method for detection of BKV that can be of use in clinical studies of this virus.

Animals↗

PubMed2003

Use of cidofovir in polyomavirus BK viral nephropathy in two renal allograft recipients.

Polyomavirus BK viral allograft nephropathy is a potentially reversible cause of deteriorating function of kidney allografts. Initial treatment involves reducing immunosuppressive medications, with low-dose cidofovir an effective alternative in refractory cases. We describe two cases of BK viral allograft nephropathy responding to low-dose cidofovir after a reduction in immunosuppressive medications failed to clear the virus or stabilize the deterioration in renal function. There were no significant side-effects from this treatment in either patient.

Antiviral Agents↗

PubMed2006

Activation of early gene transcription in polyomavirus BK by human immunodeficiency virus type 1 Tat.

Polyomavirus BK (BKV) is a serious problem for immunocompromised patients, where latent virus can enter into the lytic cycle causing cytolytic destruction of host cells. BKV infects >80% of the population worldwide during childhood and then remains in a latent state in the kidney. In the context of immunosuppression in kidney transplant patients, reactivation of the viral early promoter (BKV(E)) results in production of T antigen, enabling virus replication and transition from latency to the lytic phase, causing polyomavirus-associated nephropathy. Reactivation of BKV can also cause complications such as nephritis, atypical retinitis and haemorrhagic cystitis in AIDS patients. Here, the effects of human immunodeficiency virus type 1 (HIV-1) proteins Tat and Vpr on BKV transcription were investigated and it was demonstrated that Tat dramatically stimulated BKV(E). Site-directed mutagenesis analysis of potential Tat-responsive transcriptional motifs complemented by an electrophoretic mobility shift assay (EMSA) showed that Tat activated BKV(E) by inducing binding of the NF-kappaB p65 subunit to a kappaB motif near the 3' end of BKV(E). In addition, a sequence within the 5' UTR of BKV(E) transcripts (BKV(E)-TAR) was identified that is identical to the HIV-1 transactivation response (TAR) element. The BKV(E)-TAR sequence bound TAT in RNA EMSA assays and deletion of the BKV(E)-TAR sequence eliminated Tat transactivation of BKV(E) transcription. Thus, Tat positively affected BKV(E) transcription by a dual mechanism and this may be important in diseases involving BKV reactivation in AIDS patients.

BK Virus↗

PubMed1985

[Prevalence of antibodies against human BK polyomavirus in a general population and in dialysed patients from the province of Cordoba].

This study was carried out in order to determine the prevalence of HAI antibodies to BK polyomavirus in general population and patients under dialysis. In the general population 72% of the sera tested were positive, varying from 64% in the 0-5 years age group to 100% in the group above 40 years old. The HAI titers in the 0-5 years age group showed a characteristic "U" shaped pattern distribution. The prevalence in the dialysed patients was similar to the general population. The prevalence rates observed in both groups were not statistically significant. According to these results it can be concluded that BK polyomavirus infection is acquired during very early childhood.

Age Factors↗

PubMed2005

Co-infection of polyomavirus-BK and cytomegalovirus in renal transplant recipients.

BACKGROUND: Polyomavirus-BK (BK) is a significant cause of allograft dysfunction in renal transplant recipients. Cytomegalovirus (CMV) and BK infection are thought to be possible risk factors for one another, but no supporting data are yet available. METHODS: The authors monitored BK and CMV infection by quantitative polymerase chain reaction (PCR) in 69 renal transplant recipients with serum creatinine elevation to determine the prevalence of co-infection. In addition, 150 adult renal transplant recipients were also retrospectively analyzed for both infections. RESULTS: Of 69 recipients, 12 were plasma BK-PCR-positive. Eight of the 12 showed high BK levels (>10 copies) and BK nephropathy. Six of the 12 were also CMV-PCR-positive compared with only 3 of 57 plasma BK-negative patients (50% vs. 5.3%, P=0.001). Comparatively, the incidence of Epstein-Barr virus infection was similar in both groups (1 of 12 [8.3%] vs. 2 of 57 [3.5%], P =not significant). In addition, retrospective analysis of CMV-PCR-positivity in 150 adult renal transplant recipients showed similar results (5 of 6 in BK-PCR-positive [83%] vs. 8 of 144 in BK-PCR-negative [5.6%], P=0.00001). More plasma BK-PCR-positive patients had concomitant CMV infection than CMV-PCR-positive patients with BK infection (5 of 6 [83%] vs. 4 of 13 [31%], P=0.05). CONCLUSIONS: In conclusion, high plasma BK-positivity (>10) is significantly associated with BK nephropathy. Plasma BK-positivity is highly associated with co-infection of CMV, suggesting possible risk factors for one another. Therefore, detection of either infection strongly suggests the need to monitor for the other. This strategy may lead to the prevention of virus-induced complications by preemptive antiviral therapy in renal allografts.

Adolescent↗

PubMedDate not supplied

Malignant melanoma in a patient with polyomavirus-BK-associated nephropathy.

A possible relationship between malignant melanoma and polyomavirus-associated nephropathy in a renal transplant patient is presented. It is possible that BK polyomavirus (BKV) nephropathy and malignant melanoma developed independently. The coincidence may be related to over-immunosuppression. The presented case suggests careful oncological surveillance in patients with BKV nephropathy.

Adult↗

PubMed1978

Human polyomavirus (BK) infection and ureteric stenosis in renal allograft recipients.

Human polyomavirus (BK) was detected in two renal allograft recipients as a result of routine examination of Papanicolaou-stained smears of urinary sediment in the light microscope. Infection with this recently identified virus was confirmed by virus isolation and electron microscopy. The cytological, histological, and ultrastructural changes due to the virus are described, and virus excretion is correlated with the clinical progress of the patients and the pathological findings. The transplant ureters in both patients were found to be ulcerated and stenosed, and virus-infected cells were observed in the ureteric epithelium. We suggest that the administration of high-dose steroids in transplantation may permit active infection with human polyomavirus to occur in ureteric epithelium which has been damaged by ischaemia or inflammation.

Animals↗

PubMed2003

Human polyomavirus BK (BKV) transiently transforms and persistently infects cultured osteosarcoma cells.

Human polyomavirus BK (BKV) DNA and proteins have been detected in a number of bone tumours. We therefore investigated whether BKV infection might initiate transformation of human anchorage-dependent osteosarcoma cells in vitro. Infection of the osteosarcoma cell line U-2OS with a naturally occurring BKV strain resulted in soft agarose competent cell clones. In a subclone, designated U-2OS15E, approximately 10-20% of the cells contained episomal BKV genomes. A corresponding proportion of cells expressed BKV proteins and produced viral progeny. This proportion was not increased by BKV superinfection. Furthermore, U-2OS15E cells were resistant to SV40 infection. The transformed status of U-2OS15E cells lasted only for a few passages. However, the persistently infected cells produced infectious virions for more than 300 generations. In addition to representing a model system for persistent BKV infection, the uninfected and persistently BKV-infected cell cultures are useful tools for control and calibration of in situ BKV nucleic acid and protein detection methods.

Animals↗

PubMed1984

Prospective study of the human polyomaviruses BK and JC and cytomegalovirus in renal transplant recipients.

Forty eight renal transplant recipients were investigated prospectively for evidence of infection with the polyomaviruses BK and JC and cytomegalovirus. An active polyomavirus infection was shown in 31 patients (65%) and cytomegalovirus in 30 (62.5%). Half of the BK and JC virus infections occurred within the first three months after transplantation compared with 93% of the cytomegalovirus infections. Very late polyomavirus infections two or more years after the transplant were also shown. Cytology was useful in identifying polyomavirus but not cytomegalovirus infections, and 21 (68%) of the 31 polyomavirus infected patients excreted inclusion-bearing cells. Only three patients had symptoms possibly associated with the polyomavirus infection. One patient with BK virus infection developed ureteric stenosis and a second patient had malaise and vomiting. One patient with JC virus infection developed pericarditis and effusion. Renal function became impaired at the time of the polyomavius infection in eight patients (26%) and ureteric obstruction and pericarditis developed in two patients treated with methyl prednisolone for possible rejection. At the end of the study 25 of the 31 polyomavirus infected patients (81%) had functioning renal grafts. The detection of polyomavirus infection is important as increased immunosuppression needs to be avoided to prevent possible complications such as ureteric stenosis in transplant recipients.

Adolescent↗

PubMed2003

Characterization of self-assembled virus-like particles of human polyomavirus BK generated by recombinant baculoviruses.

The major structural protein of the human polyomavirus BK (BKV), VP1, was expressed by using recombinant baculoviruses. A large amount of protein with a molecular mass of about 42 kDa was synthesized and identified by Western blotting. The protein was detected exclusively in the nuclei by immunofluorescent analysis and it was released into culture medium. The expressed BKV VP1 protein was self-assembled into virus-like particles (BK-VLPs) with two different sizes (50 and 26 nm in diameter), which migrated into four different bands in CsCl gradient with buoyant densities of 1.29, 1.30, 1.33, and 1.35 g/cm(3). The immunological studies on the BK-VLPs suggested that they have similar antigenicity with those of authentic BKV particles. Cryoelectron microscopy and 3D image analysis further revealed that the larger BK-VLPs were composed of 72 capsomers which all were pentamers arranged in a T = 7 surface lattice. This system provides useful information for detailed studies of viral morphogenesis and the structural basis for the antigenicity of BKV.

Amino Acid Sequence↗

PubMed2003

BK polyomavirus: a newly recognized threat to transplanted kidneys.

Reactivation of latent infection with BK polyomavirus is now being recognized as a cause of failure of renal allografts. An increasing serum creatinine concentration in a kidney transplant recipient should prompt a referral for reevaluation by the transplant center.

BK Virus↗

PubMed2005

[Polyomavirus BK infection in renal transplant recipients].

Beside acute rejection or immunosuppressive therapy toxicity, infection by Polyomavirus BK, usually not aggressive in immunoactive patients, has emerged as an important factor affecting graft function in renal transplant recipients. Indeed, one of the most important complications of BK infection is nephropathy. Viral replication in the urinary tract as assessed by the presence of "decoy cells", or by a positive PCR for BK virus has been detected in up to half of the recipients but only 5% will present nephropathy which is usually the only sign. The most common risk factors for this emerging new cause are new immunosuppressive drugs and rejection episodes. The gold standard to diagnose BK nephropathy is immunohistochemical staining for large T antigen in graft biopsy specimens. Urine cytology examination and DNA BK PCR are used as a screening test. The prognosis in BK nephropathy has been considered to be poor. The early reduction of immunosuppression can improve the prognosis and perhaps also cidofovir or leflunomide use.

Adult↗

PubMed1998

The agnogene of the human polyomavirus BK is expressed.

Primate polyomavirus genomes all contain an open reading frame at the 5' end of the late coding region called the agnogene. A simian virus 40 agnoprotein with unknown functions has previously been demonstrated. We now show that a BK virus agnoprotein appears in the perinuclear area and cytoplasm late in the infectious cycle. It is phosphorylated in vivo and coimmunoprecipitates with a subset of host cell proteins.

BK Virus↗

PubMed2005

Quantitation of DNA of polyomaviruses BK and JC in human kidneys.

BACKGROUND: Renal allograft recipients can be monitored for polyomavirus-associated nephropathy (PVAN) using urine samples. Because virus in urine can be derived from the kidneys, ureter, or urinary bladder, we evaluated whether measurement of intrarenal concentrations of viral DNA might serve as a more reliable monitoring tool. METHODS: Real-time quantitative polymerase chain reaction was used to quantitate DNA of polyomaviruses BK (BKV) and JC (JCV) in renal tissue obtained from various clinical settings. RESULTS: Renal biopsy samples from 28 nonimmunosuppressed patients contained very low viral copy numbers. Minimally higher BKV loads (mean +/- SE, 3.4 +/- 1.7 copies/cell) were observed in 74 renal biopsy samples from renal allograft recipients with BKV viruria. The BKV DNA concentration was approximately 10-fold higher in renal allograft recipients with BKV viruria, but 58 (50.4%) of 115 renal biopsy samples tested negative for BKV DNA, reflecting the focal nature of infection. JCV DNA was found in only 2 renal biopsy samples. CONCLUSIONS: The BKV load is better measured in urine than in tissue, because a urine sample represents material from the entire kidney. An increase in the BKV load is usually not accompanied by a proportional increase in the JCV load, which indicates that these 2 related polyomaviruses are subject to different mechanisms regulating viral replication.

BK Virus↗

PubMed2006

Subtype I BK polyomavirus strains grow more efficiently in human renal epithelial cells than subtype IV strains.

BK polyomavirus (BKPyV) is ubiquitous in human populations, infecting children without obvious symptoms and persisting in the kidney. BKPyV isolates have been classified into four subtypes (I-IV) using either serological or genotyping methods. In general, subtype I occurs most frequently, followed by subtype IV, with subtypes II and III rarely detected. As differences in growth capacity in human cells possibly determine the proportion of the four subtypes of BKPyV in human populations, here the growth properties of representative BKPyV strains classified as subtype I or IV in renal proximal tubule epithelial cells (HPTE cells) of human origin were analysed. HPTE cells were transfected with four and three full-length BKPyV DNAs belonging to subtypes I and IV, respectively, and cultivated in growth medium. Virus replication, detected using the haemagglutination assay, was observed in all HPTE cells transfected with subtype I BKPyV DNAs, whereas it was markedly delayed or not detected in those transfected with subtype IV BKPyV DNAs. It was confirmed that the transfected viral DNAs induced virus replication in HPTE cells. Furthermore, it was found that BKPyVs with archetypal transcriptional control regions replicated in HPTE cells, with only the occasional emergence of variants carrying rearranged transcriptional control regions. Essentially the same results as described above were obtained with renal epithelial cells derived from whole kidney. Thus, it was concluded that subtype I BKPyV replicates more efficiently than subtype IV BKPyV in human renal epithelial cells, supporting the hypothesis that growth capacity in human cells is related to the proportion of BKPyV subtypes in human populations.

BK Virus↗

PubMed1996

Duplex polymerase chain reaction for the simultaneous detection of the human polyomavirus BK and JC DNA.

With the aim of further simplifying the detection of human polyomaviruses BK (BKV) and JC (JCV), by reducing the time and the cost of the reactions, a duplex polymerase chain reaction (PCR) was developed for the simultaneous detection and identification of BKV and JCV DNA. A nested PCR was performed. In a first amplification reaction the same set of primers was used to amplify a sequence of either BKV or JCV genomes. Two sets of primers, each specific for BKV or JCV DNA, were used in a second amplification. The products of BKV and JCV DNA amplification were distinguishable on the basis of their different size. The sensitivity and the specificity of the duplex PCR was shown to be exactly comparable to that of the single PCR, not only with the BKV and the JCV plasmid but also for BKV and JCV DNA detection in clinical specimens.

BK Virus↗

PubMed2006

Characterization of highly frequent epitope-specific CD45RA+/CCR7+/- T lymphocyte responses against p53-binding domains of the human polyomavirus BK large tumor antigen in HLA-A*0201+ BKV-seropositive donors.

Human polyomavirus BK (BKV) has been implicated in oncogenic transformation. Its ability to replicate is determined by the binding of its large tumor antigen (LTag) to products of tumor-suppressor genes regulating cell cycle, as specifically p53. We investigated CD8+ T immune responses to BKV LTag portions involved in p53 binding in HLA-A*0201+ BKV LTag experienced individuals. Peptides selected from either p53-binding region (LTag351-450 and LTag533-626) by current algorithms and capacity to bind HLA-A*0201 molecule were used to stimulate CD8+ T responses, as assessed by IFN-gamma gene expression ex vivo and detected by cytotoxicity assays following in vitro culture. We observed epitope-specific immune responses in all HLA-A*0201+ BKV LTag experienced individuals tested. At least one epitope, LTag579-587; LLLIWFRPV, was naturally processed in non professional antigen presenting cells and induced cytotoxic responses with CTL precursor frequencies in the order of 1/20'000. Antigen specific CD8+ T cells were only detectable in the CD45RA+ subset, in both CCR7+ and CCR7- subpopulations. These data indicate that widespread cellular immune responses against epitopes within BKV LTag-p53 binding regions exist and question their roles in immunosurveillance against tumors possibly associated with BKV infection.

Journal Article↗