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At least 19 recordsLinked to original sources

PubMed2026

Binding capacity of Intravenous immunoglobulin G to BK polyomavirus determines its anti-BK polyomavirus activity in infected cultures.

BK polyomavirus (BKPyV) causes disease in immunocompromised individuals. This study tested the hypothesis that the antiviral efficacy of intravenous immunoglobulin (IVIG) against BKPyV depends on the relationship between its virus-binding capacity and the viral burden. We first quantified the BKPyV-binding capacity of IVIG and then characterized BKPyV replication in kidney-derived HK-2 and HEK293 cells and in HEL cells under IVIG treatment. Subsequently, we analyzed the efficacy of IVIG at 0.03-10 mg/mL against low-multiplicity of infection (MOI) and high-MOI infection in relation to the BKPyV-binding capacity of IVIG. BKPyV productively infected all three cell lines, with 14-day replication cycles of 2.2, 4.0, and 7.0 in HK-2, HEK293, and HEL cells, respectively, indicating that HEL cells were the most permissive. IVIG bound approximately 108 copies of BKPyV DNA per milligram. In the low-MOI infection model, where the total viral load remained within this estimated binding capacity, IVIG showed clear neutralizing activity, significantly reducing viral spread, viral DNA levels, and the number of VP1-positive cells in a dose-dependent manner (p < 0.001). In contrast, in the high-MOI infection model, the viral load appeared to be high relative to the estimated IVIG binding capacity even at 10 mg/mL, and IVIG showed little or no neutralizing effect on viral production or spread of infected cells. These findings identify an experimental relationship between IVIG binding capacity, viral burden, and antiviral efficacy and suggest that the antiviral effect of IVIG is greatest when administered early, thereby supporting further clinical evaluation of early or preemptive IVIG administration.

Humans↗

PubMed2026

Genetic Diversity of BK Polyomavirus Among Renal Transplant Recipients in Yunnan, China.

BK polyomavirus (BKV) infection, a common complication following kidney transplantation, can lead to BKV-associated nephropathy (BKVN). Molecular genetic studies have classified BKV into four genotypes (I-IV); however, comprehensive molecular characterization of BKV strains circulating in China remains limited. This study aimed to elucidate the predominant subtypes and clinical infection characteristics of BKV strains among kidney transplant recipients in Yunnan, a province in southwestern China. PCR-amplified BKV DNA sequences from kidney transplant recipients were aligned with reference strains and subjected to phylogenetic analysis. The viral VP1 gene was successfully amplified from 180 participants, spanning 16 ethnic groups. Genotype I was the predominant viral strain (56.66%, 102/180), followed by genotype IV (43.33%, 78/180), while genotypes II and III were not detected. Among genotypic subtypes, IVc-1 was most prevalent (40.0%, 72/180), followed by Ic (38.3%, 69/180) and Ib-1 (18.3%, 33/180). IVa-1 and IVa-2 were rare, identified in only 0.6% (n = 1) and 2.2% (n = 4) of cases, respectively. No significant differences in sex, age, BKVN incidence, BK viremia, or viruria were observed between patients with BKV-I and BKV-IV infections. Among the five confirmed BKVN cases, two were genotyped as subtype Ic, one as Ib-1, and two as IVc-1. Clinical phenotypes were also comparable between patients with BKV-I and BKV-IV infections. This study represents the largest single-center sequencing analysis of BKV in kidney transplant recipients in China, offering a valuable genomic resource for future research.

Humans↗

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↗

PubMed1991

Proteins of the nuclear factor-1 family act as an activator of the late promoter in human polyomavirus BK in vitro.

The cis-acting elements for the early and late promoters, as well as the enhancer in the prototype strains of human polyomavirus BK (BKV) are located within a 500 bp intergenic region. We previously studied the specificity of protein binding in this region in vitro and showed that the interaction of proteins of the nuclear factor-1 (NF-1) family is crucial for early promoter activity. We have now extended our study to the BKV late promoter. We show that the late promoter activity in HeLa cell extracts is poor compared to the activity of the early promoter. Using a high template to protein ratio, multiple start sites were detected by primer extension analysis. DNase I protection experiments revealed the presence of three NF-1 binding sites in the late side, in addition to those identified previously in the 68 bp repeats and C element. Competition transcription assays using binding sites for NF-1, AP-1, Sp-1 and a complete 68 bp repeat indicated that only the 68 bp repeat and the NF-1 binding site competed significantly with the late promoter activity. A point mutation in the NF-1 binding site, which destroys the ability of the oligonucleotide to bind NF-1, also impaired its capacity to compete with the late promoter. The ability of NF-1 to activate both the early and late promoters suggests that the proteins of this family act as a bidirectional transcriptional activator in this virus.

BK Virus↗

PubMed1991

[New human polyomavirus; BK virus antibody levels in different age groups using the hemagglutination inhibition test].

In this study, 1123 human sera samples obtained from healthy persons belonging to various age groups were tested in order to detect the distribution of antibody levels against the new human polyomavirus, BK. All sera samples were tested by hemagglutination inhibition (HI) test and 881 (78.5%) of those were found to be positive and 242 (21.5%) were negative. The percentage of positivity was 65.3% between the ages of 1 to 5 years, and over 80% in the group aged 6 years or older. Furthermore, between 1 to 10 years of ages HI antibody titers were higher than the older age groups. Our results indicate that antibody to BK virus infections are remarkably frequent in our population and acquisition of BK virus appeared to be common in childhood.

Adolescent↗

PubMed1975

Evidence of chronic persistent infections with polyomaviruses (BK type) in renal transplant recipients.

Ten renal transplant recipients showing a significant increase in human polyomavirus antibodies, indicative of an acute infection, were followed up serologically over periods ranging from two months to more than two years. Fifty-four serum specimens were available for the study and they were tested by both haemagglutination-inhibition and complement-fixation. Polyomavirus antigens were prepared from the BK and SV40-like strains of polyomaviruses, and from the SV40 virus. One strain of polyomavirus, related to the BK strain was isolated from the urine of one of these patients. Two other BK strains were recovered from the urine and kidney, respectively, of transplant recipients not included in this study. Sera of these two patients were not obtained until the transplantation was made; they were already highly positive for polyomavirus antibodies, precluding the demonstration of an increase in antibody titer. Serologic results have shown that HAI antibodies persist at high titers throughout the observation period. This persistence ranged from two to four months (four cases), seven to eleven months (three cases) and thirteen to twenty months (three cases). In none of the cases could a decrease of high titer be demonstrated. Moreover, density gradient studies have shown that specific IgM antibodies also tend to persist over many months. Similar serologic results were obtained in complement-fixation tests with a BK antigen. Titers were at least 1 in 30 in the study group, but were not observed among healthy blood donors. All sera were uniformly negative for SV40 and SV40-like antigens. One polyomavirus isolation was successful from urine obtained six months after initial serologic evidence for a polyomavirus infection. The other two viruses were isolated from materials taken four and seven months after first detection of polyomavirus antibodies at high titer. Both serologic evidence and viral isolations seem to indicate that polyomaviruses (BK type) might cause a chronic infection in humans.

Animals↗

PubMed1992

Evidence of human polyomavirus BK and JC infection in normal brain tissue.

Infection with the polyomaviruses JC and BK is ubiquitous in the human population and JCV is the only virus associated with the central nervous system disease progressive multifocal leukoencephalopathy. In the attempt to analyze the pathogenesis of polyomavirus infections we asked whether human polyomaviruses invade the brain during persistence. Brain autopsy material from 67 individuals with disorders other than PML was examined for the presence of polyomavirus DNA. Southern blot analysis demonstrated JCV-specific full-length virus genomes in healthy brain tissue in about 20% of the patients. Type-specific analysis with polymerase chain reaction and sequencing confirmed these data. Additionally, the presence of BKV DNA sequences covering an early gene fragment and the control region with flanking early and late protein coding sequences was detected. Cloning of the complete BKV genome from two cases supported the assumption that not only full-length JCV DNA was present in those tissue specimens but also BKV genomes. The data obtained demonstrate that dual infection of the brain with the polyomaviruses JCV and BKV is a common event and give strong evidence that both viruses frequently establish a latent CNS infection.

BK Virus↗

PubMed2026

Benchmarking urinary cell transcriptomes for noninvasive differentiation of BK polyomavirus-associated nephropathy from T cell-mediated rejection.

BK polyomavirus-associated nephropathy (BKVN) adversely impacts kidney allograft survival and often mimics acute T cell-mediated rejection (TCMR), confounding diagnosis and management. To address this conundrum, we performed unbiased RNA sequencing of urinary cells matched to biopsies classified as BKVN with intragraft inflammation (BKVN-P), BKVN without inflammation (BKVN-N), TCMR, or no rejection (NR). BKVN-N displayed dominant host DNA replication, cell cycle, and repair programs, while BKVN-P samples exhibited expansive innate immune activation, antigen presentation, chemokine upregulation, and epithelial injury. Both BKVN subtypes shared signatures of T cell exhaustion and mature and tolerogenic dendritic cell activation but differed in immune orientation - Th1 predominance in BKVN-N versus Treg and CD8 enrichment in BKVN-P. Compared with TCMR samples, BKVN-P lacked robust TCR/CD28 signaling and was enriched for viral and innate modules; BKVN-N lacked alloimmune activation. B cell exhaustion characterized BKVN-N, while BKVN-P displayed robust B cell activation with metabolic downregulation. A ratiometric urinary cell biomarker, CXCL10 mRNA/CD3E mRNA, distinguished both BKVN subtypes from TCMR with diagnostic accuracy, replicated by quantitative reverse transcription PCR for clinical translation, and confirmed in an independent cohort. These findings demonstrate the utility of urinary cell transcriptomics for resolving viral injury from alloimmunity, enabling precision diagnostics and targeted immunomodulation in kidney transplantation.

Humans↗

PubMed2026

Single-cell profiling reveals epithelial and immune responses in BK polyomavirus-infected human kidney biopsies.

INTRODUCTIONBK polyomavirus (BKV) infection is associated with injury and subsequent graft loss due to the extent of injury or rejection. However, the molecular mechanisms driving injury and subsequent adverse outcomes remain poorly understood.METHODSIn a cross-sectional study, single-cell RNA-seq from kidney allograft biopsies was used to assess cell type-specific responses between uninfected controls and 2 distinct phases of BKV infection: peaking (increasing viral blood titers) and resolving (decreasing viral titers following immunosuppression reduction).RESULTSGenes upregulated in BK viral nephropathy (BKVN) were enriched for polyomavirus infection hallmarks, including ribosome biogenesis, translation, and energy restructuring. Additionally, enriched pathways included wound healing, cellular stress, antigen presentation and immune signaling. Even without BKVN (peaking BK viremia alone), epithelial cells expressed signatures for wound healing, cellular stress, and extracellular matrix remodeling. In vivo tubular cell responses at single-cell resolution were validated against single cell transcriptomic data of BKV-infected cells in a cell culture model. Despite similarities, in vivo tubular cells underwent metabolic adaptation favoring fatty acid oxidation and proinflammatory responses not observed in culture models, likely due to an absent innate and adaptive immune system. Despite lymphopenia and immunosuppressive therapies, the proportion of recipient-derived intrarenal adaptive immune cells was increased in biopsies associated with peaking viremia alongside activation of innate immune responses. Adaptive immune cells exhibited persistent inflammatory signaling and remodeling of energy metabolism during the resolving phase of infection.CONCLUSIONThese not previously reported insights into BKV-associated injury may have implications for clinical management and improved allograft outcomes.

Humans↗

PubMed2025

Identification of Novel Wraparound Transcripts in JC Polyomavirus.

JC polyomavirus (JCPyV) is a ubiquitous pathogen that causes progressive multifocal leukoencephalopathy (PML). Although a recent study using next-generation sequencing (NGS) provided detailed transcriptome atlases for polyomaviruses (PyVs) such as BK polyomavirus and simian virus 40, the transcriptome of JCPyV remains poorly characterized. Here, we conducted a comprehensive analysis using both short-read and long-read NGS technologies to construct a transcriptome atlas of JCPyV. RNA extracted from IMR-32 and HEK293 cells transfected with the circular JCPyV genome was analyzed, leading to the identification of 39 previously uncharacterized viral transcripts in addition to 12 known ones. Among the novel transcripts, we identified wraparound transcripts, conserved across PyVs, which are generated through continuous, multicyclic transcription of the circular viral genome. These included both late transcripts containing leader-to-leader repeated sequences and SuperT transcripts with multiple LxCxE motifs. Notably, wraparound transcripts, including SuperT transcripts, were also detected in brain tissues from PML patients. Collectively, this study significantly expands our understanding of the JCPyV transcriptome, revealing the expression of wraparound transcripts in PML lesions. These findings provide valuable insights into the molecular basis of JCPyV gene expression and PML pathogenesis, potentially facilitating the development of effective countermeasures against PML.

JC Virus↗

PubMed1992

DNA sequences similar to those of simian virus 40 in ependymomas and choroid plexus tumors of childhood.

BACKGROUND: Ependymomas and papillomas of the choroid plexus occur in early childhood. The ubiquitous human polyomaviruses, BK virus and JC virus, have been associated with the induction of these neoplasms in animal models. A related monkey polyomavirus, simian virus 40 (SV40), is highly tumorigenic in rodents and also induces choroid plexus papillomas. METHODS: We tested the possibility that polyomaviruses were associated with these tumors in humans. Tumors from 31 children--20 with choroid plexus neoplasms and 11 with ependymomas--were evaluated for the presence of polyomavirus T-antigen gene sequences by means of amplification with the polymerase chain reaction. RESULTS: Ten of the 20 choroid plexus tumors and 10 of the 11 ependymomas contained amplification products that preferentially hybridized to probes specific for SV40 viral DNA rather than BK or JC viral DNA. In two specimens, DNA sequencing demonstrated that the amplified sequence was identical to the sequence of that region of the SV40 gene. In three other specimens, amplification with SV40-specific primers revealed a 574-bp segment of the SV40 viral gene. In 7 of 11 tumors examined by immunohistochemical staining, viral T antigen was expressed in the nuclei of the neoplastic cells. CONCLUSIONS: Half of the choroid plexus tumors and most of the ependymomas that we studied contained and expressed a segment of T-antigen gene related to SV40. These results suggest that SV40 or a closely related virus may have an etiologic role in the development of these neoplasms during childhood, as in animal models.

Antigens, Viral, Tumor↗

PubMed1991

Antibodies against BK virus in renal transplant recipient sera: results with five different methods indicate frequent reactivations.

Sera from 10 renal transplant recipients were investigated longitudinally for antibodies to human polyomavirus BK (BKV) using specific IgG-, IgA- and IgM-ELISA, hemagglutination inhibition (HAI) and neutralization tests (NT). Nine patients had anti-BKV serum antibodies before transplantation. The serological findings in 5 patients were compatible with reactivation of BKV infections. The results obtained with different tests were generally in good agreement. However, according to the definition of significant titer increase. 1-3 patients would have been undetected by employing HAI alone. High levels of antibodies detected by the other tests generally corresponded well with NT titers, i.e. the ability to neutralize infectivity. All the 5 patients with reactivation also showed an increase in specific IgA antibodies.

Adult↗

PubMed1991

Hemorrhagic cystitis after bone marrow transplantation: importance of a thin sectioning technique on urinary sediments for diagnosis.

We used a thin-sectioning technique for the electron microscopic detection of viral particles within the cells of urinary sediments in three recipients who developed hemorrhagic cystitis after allogeneic bone marrow transplantation. Results of viral cultures of urine and electron microscopic (EM) observations on urinary sediments were consistent in only one recipient. In this recipient, EM observations revealed many viral particles within the cells of urinary sediments with diameter of about 80 nm corresponding to adenovirus, of which type 11 was produced in viral cultures. In one of the other two recipients many viral particles with a mean diameter of 41.6 nm corresponding to papovavirus were observed, but viral cultures using conventional cells were negative. Re-cultures using HEK cells produced polyomavirus BK. EM observation was a clue to the correct diagnosis. In the remaining recipient, no viral particles were observed within the cells of urinary sediments, suggesting the hemorrhagic cystitis to be of non-viral origin, despite a positive result of viral culture. These results suggest that a thin-sectioning technique on the cells of urinary sediments is important for the differential diagnosis between a viral-induced and non-viral hemorrhagic cystitis.

Adenoviridae↗

PubMed1992

PAb 2000 specifically recognizes the large T and small t proteins of JC virus.

A monoclonal antibody, PAb 2000, has been derived which recognizes the large T protein of JC virus (JCV), but not the corresponding proteins of the related polyomaviruses BK virus (BKV) and SV40. The epitope bound by PAb 2000 was localized to the amino-terminal 81 amino acids of this multifunctional protein. As observed previously with several monoclonal antibodies that bind a similar region of SV40 large T antigen, PAb 2000 was found to interact with the small t antigen and the denatured form of large T antigen. This monoclonal antibody recognized a subpopulation of T protein, the abundance of which varied in different species of cells transformed by JCV. The availability of PAb 2000, the first JCV T antigen-specific monoclonal antibody, will facilitate the purification and biochemical characterization of the JCV oncoproteins.

Animals↗

PubMed1992

Five DNA tumor viruses undetectable in human retinoblastomas.

Retinoblastoma (RB) is a childhood eye cancer that arises when a retinal cell lacks a functional RB gene. Recent data indicate the transforming proteins of adenovirus, papillomavirus, and the polyomaviruses BK and JC all can bind to the product of the RB gene. Furthermore, adenovirus 12, JC virus, and simian virus 40 are able to induce RB-like tumors in rodents. In view of these findings, 50 human RBs were tested for the presence of five human DNA tumor viruses: adenovirus 12, BK virus, JC virus, and human papillomaviruses 16 and 18. Using the polymerase chain reaction, no viral sequences were detected in 50 RB DNAs. These data provide no evidence that these viruses have an etiologic role in human RB.

Base Sequence↗

PubMed1991

Survey of urine from transplant recipients for polyomaviruses JC and BK using the polymerase chain reaction.

Using polymerase chain reaction (PCR), we examined 108 urine specimens from 39 post transplant patients for polyomaviruses JC (JCV) and BK (BKV). Urine sediments were collected and subjected to 30 cycles of amplification. PCR products were resolved by agarose gel electrophoresis, transferred to nylon membranes by Southern blot, and hybridized with radiolabelled probes. Polyomavirus DNA was found in urine specimens from 17 out of 39 patients (44%). Both viruses were detected in specimens from nine patients, JCV alone in five, and BKV alone in three. In comparison, polyomavirus was detected in only five of 22 PCR positive specimens by shell vial cell culture assay. Our results show a high prevalence of polyomavirus shedding after transplantation and suggest a higher rate of JC viruria than previously reported.

DNA, Viral↗

PubMed1992

[BK and JC viruses--2 polyomaviruses causing disease in immunosuppressed patients].

BK and JC viruses are two polyoma viruses designated by the initials of the patients from whom they were first isolated. After the primary infection, usually occurring in childhood or early school age, the viruses become latent. Reactivation occurs during immunosuppression, and the BK virus has been shown to be the main cause of viral hemorrhagic cystitis in bone marrow transplanted patients, while the JC virus has been found to cause progressive multifocal leukoencephalopathy, PML. The paper consists in a report of results obtained with an established method for the amplification of BK and JC virus DNA. Of 20 urine specimens from patients with hemorrhagic cystitis, 13 were found to be BK virus-positive. Post-transplantation follow-up shows that the virus continues to remain detectable for long periods. JC virus positivity was found in central nervous system material (a cerebrospinal spinal fluid specimen in one case) from two PML patients.

BK Virus↗

PubMed1991

The use of vidarabine in the treatment of human polyomavirus associated acute haemorrhagic cystitis.

The human BK and JC polyomaviruses are known to be reactivated and excreted in the urine following bone marrow transplantation (BMT). A proportion of patients who excrete BK virus following BMT experience a haemorrhagic cystitis (HC), which may persist for many months. We report a case of human polyomavirus-associated HC, in whom treatment with vidarabine was associated with a dramatic response.

Acute Disease↗