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At least 19 recordsLinked to original sources
PubMed2006

Urine cytology findings of polyomavirus infections.

Polyomaviruses of the BK- and JC-strains often remain latent within the transitional cell layer of the bladder, ureters and the renal pelvis as well as in tubular epithelial cells of the kidney. Slight changes in the immune status and/or an immunocompromised condition can lead to the (re)activation of latent polyomaviruses, especially along the transitional cell layer, resulting in the shedding of viral particles and infected cells into the urine. A morphologic sign of the (re)activation of polyomaviruses is the detection of typical intranuclear viral inclusion bearing epithelial cells, so-called "decoy cells", in the urine. Decoy cells often contain polyoma-BK-viruses. The inclusion bearing cells are easily identified and quantifiable in routine Papanicolaou stained urine cytology specimens. With some experience, decoy cells can also be detected in the unstained urinary sediment by phase contrast microscopy. Different morphologic variants of decoy cells (types 1 through 4) are described and ancillary techniques (immunohistochemistry, electron microscopy (EM), and fluorescence-in-situ-hybridization (FISH)) for proper identification and characterization are discussed. Special emphasis is placed on the clinical significance of the detection of decoy cells as a parameter to assess the risk for disease, i.e., polyoma-BK-virus nephropathy (BKN) in kidney transplant recipients. The sensitivity and specificity of decoy cells for diagnosing BKN is 99% and 95%, respectively, the positive predictive value varies between 27% and more than 90%, and the negative predictive value is 99%. The detection of decoy cells is compared to other techniques applicable to assess the activation of polyomaviruses in the urine (polymerase chain reaction (PCR) and EM).

Cytodiagnosis↗
PubMed1998

Cytologic and genetic study of polyomavirus-infected or polyomavirus-activated cells in human urine.

OBJECTIVE: To carry out a morphologic and genetic study of human polyomavirus infection or activation in child and adult urine specimens. DESIGN AND SETTING: The study was carried out on 16 urine samples from children with human polyomavirus infection and 104 samples from adults with virus activation identified among 18800 consecutive urine samples (0.64%). RESULTS: All specimens from children showed numerous typical intranuclear inclusion-bearing (INIB) cells. All adult specimens with cytological features similar to childhood specimens were defined as type 1 adult cases. We identified 14 adult cases with marked immunologic suppression as type 1 cases. The inclusions were large, homogeneous, and basophilic, and they were mainly attributable to the BK virus, as demonstrated by a polymerase chain reaction. These infected or activated cells revealed features demonstrating their origin in the superficial transitional epithelium of the urinary tract. Adult cases with different cytologic features were designated as type 2 adult cases. In type 2 adult cases, the number of virus-activated cells was lower, and degenerated intranuclear inclusion-bearing cells with a coarse chromatin pattern were observed in most cases. These characteristics were identified in 90 adults without immunologic suppression. A polymerase chain reaction with BamHI digestion demonstrated JC virus DNA in nearly all of these specimens. CONCLUSION: The JC virus-activated cells found in type 2 adult cases and the BK virus-infected cells found in childhood cases were not of clinical importance. However, the BK virus-activated cells associated with immunologic suppression may have prognostic significance.

Adult↗
PubMed2003

Role of sialic acid-containing molecules and the alpha4beta1 integrin receptor in the early steps of polyomavirus infection.

Murine polyomavirus (MPyV) infection occurs through recognition of sialic acid (SA) residues present on the host cell membrane, but the nature of the molecules involved and the exact role of this interaction in virus cell entry still need to be clarified. In this work, mutations at residues R(77) or H(298) of the MPyV VP1 protein were shown to lead to a complete loss of virus infectivity, which, however, could be restored by lipofection of virus particles into the cytoplasm of the host cells. Using virus-like particles (VLPs), it was demonstrated that the non-infectivity of these mutants was due to impaired cell entry caused by total abrogation of SA-dependent cell binding. This indicates that SA residues are essential primary cell receptors for MPyV. As the alpha4beta1 integrin has been identified recently as a cell receptor for MPyV, the relationship, if any, was investigated between SA-containing and alpha4beta1 integrin receptors. The ability of mutants R(77)Q and H(298)Q and wt VLPs to bind to cells overexpressing the alpha4beta1 integrin was studied in SA-positive (BALB/c 3T3 cells and Pro-5 cells) and SA-deficient (Pro5-derived Lec-2 cells) backgrounds. Overexpression of alpha4beta1 integrin did not restore binding of mutant VLPs in any of these cell lines or, indeed, that of wt VLPs in a SA-deficient background. Moreover, evidence is provided that overexpression of the sialylated alpha4beta1 integrin enhances wt VLP cell binding, suggesting that, in addition to its function at a post-attachment level, alpha4beta1 integrin acts also as one of the SA-containing receptors for initial cell binding.

3T3 Cells↗
PubMed1988

Immunosuppression and murine polyomavirus infection.

Murine polyomavirus (MPYV) infection in mice has many similarities to human infections by BK virus (BKV) and JC virus (JCV) and provides a model for the human infections. MPYV causes acute, inapparent infection with virus appearing in numerous organs, including brain and kidney, and then subsides and becomes latent. At a later time it can be reactivated by corticosteroid treatment or pregnancy (McCance and Mims, 1979, McCance, 1983). To determine the effect of prolonged immunosuppression on virus activity in brain and kidney during acute infection, mice were treated with methotrexate, cyclophosphamide, or prednisone and azathioprine and inoculated with murine polyomavirus. Prednisone/azathioprine and cyclophosphamide caused protracted kidney infection and methotrexate had no effect. In the brain, prednisone/azathioprine and cyclophosphamide had minor effects on virus titers and course of infection, but methotrexate prevented MPYV from appearing in the brain. When mice were immunosuppressed with prednisone/azathioprine one week prior to inoculation, titers were much higher in the kidneys, but virus did not appear in the brain until late in the course of infection.

Animals↗
PubMed2006

Quantitative real-time PCR assay for detection of human polyomavirus infection.

The human polyomaviruses BK (BKV) and JC (JCV) affect immunosuppressed patients and are associated with urogenital tract (BKV) and CNS disorders (JCV) and in humans, the pathogenic role of the rhesus monkey virus, Simian virus 40 (SV40), is uncertain. These three viruses have somewhat overlapping tissue pathogenicity and detection of all three polyomaviruses is desirable. A broadly targeted, simple, single tube real-time degenerated quantitative PCR (QPCR) technique for detection of JCV, BKV and SV40 DNA was developed. To avoid false positive results, due to contamination with commonly used SV40 T-antigen plasmids, a conserved region of the VP2 gene was targeted. Down to 1-10 copies of target DNA per PCR reaction were detected. The QPCR was compared with a nested PCR on 41 clinical samples (urine, serum and plasma): 24 (58.5%) tested positive by nested PCR, whereas 31 (75.6%) were positive with QPCR. One CSF sample, from a patient with progressive multifocal leukoencephalopathy, was negative with the nested PCR but determined as positive by QPCR. Sera from 24 blood donors were negative with QPCR. The QPCR described had a high sensitivity. Its specificity was confirmed sequencing. The QPCR is simple to perform and is valuable for diagnosis of polyomavirus infection.

BK Virus↗
PubMed1980

Human polyomavirus infections with JC virus and BK virus in renal transplant patients.

Infection with the human polyomaviruses JC virus and BK virus was studied in 61 immunosuppressed renal transplant patients. Urine cytologic studies, indirect immunofluorescence microscopy, electron microscopy, and serologic studies were used to assess viral activity. Patients records were abstracted for events associated with polyomavirus infections. Polyomavirus excretion in urine was detected in 12 of 61 patients (20%). Eleven excreted JC virus and nine, BK virus. Fourfold hemagglutination-inhibition antibody titer rises occurred in 25 of 61 patients (41%). The serologic data suggested that most JC virus infections were primary, whereas most BK virus infections resulted from virus reactivation. During this 2-year study, 32 of 61 patients (52%) had evidence of active viral replication. Urinary tract excretion was associated with drug-requiring diabetes mellitus (P = 0.001), arterial occlusive disease (P = 0.03), and ureteral stricture with loss of renal function (P = 0.02). Antibody increases to BK virus were associated with a rising seurum creatinine (P = 0.02) and need for transplant biopsy (P = 0.02). Polyomavirus replication was therefore associated with an increased frequency of transplant related complications.

Adolescent↗
PubMed1999

[Polyomavirus infections in exotic birds in Switzerland].

Polyomavirus infections in budgerigars, in other parrots as well as in passeriformes have been described in many countries, but not in Switzerland so far. This paper reports on cases of polyomavirus infections in three different bird collections in Switzerland. The first outbreak occurred in a mixed collection of passeriformes, the second in a collection of parrotlets (Genus Forpus), and the third in a large groups of parrots (Psittaciformes), of which only one recently acquired Kea (Nestor notabilis) was affected. The clinical symptoms, gross necropsy changes and histopathologic findings are described. The presence of avian polyomavirus was confirmed by the polymerase chain reaction (PCR).

Animals↗
PubMed2004

Pathogen-host standoff: immunity to polyomavirus infection and neoplasia.

Polyomaviruses establish persistent infection in a variety of hosts, including humans, where they pose an oncogenic threat under conditions of depressed immune function. Control of persistent infection by these DNA tumor viruses requires continuous immunosurveillance by functionally competent antiviral CD8+ T cells. Repetitive antigen encounter by these T cells, however, often leads to their deletion or inactivation. Elucidation of the in vivo mechanisms that sustain antigen-specific CD8+ T-cell effector activity in the face of persistent antigen is essential for devising immunotherapeutic strategies against viral oncogenesis.

Animals↗
PubMedDate not supplied

Adult X-linked immunodeficiency (XID) mice, IGM-/- single knockout and IGM-/- CD8-/- double knockout mice do not clear polyomavirus infection.

The importance of antibodies for elimination of polyomavirus infection and the prevention of virus induced oncogenesis was studied, X-linked immunodeficiency (XID) mice, IgM-/- single knockout and IgMI-/- CD8-/- double knockout mice, all defective in antibody production, and normal control mice were infected with polyomavirus as adults. The mice were followed for presence of polyoma DNA with a polyoma specific polymerase chain reaction (PCR) over 6 weeks post infection (p.i.), a time point at which polyomavirus DNA is no longer detected in normal adult infected mice. As expected, virus DNA was not detected in normal mice 6 weeks p.i. In both IgM-/- single knockout and IgM-/- CD8-/- double knockout mice a disseminated infection was still observed by 6 weeks p.i. and the latter group of mice succumbed around two months p.i. In XID mice, only one third of the mice were still positive for viral DNA 6 weeks p.i. No polyomavirus induced tumors were observed in any of the mice during the 2-4 month observation period.

Animals↗
PubMed2000

Polyomavirus-infected dendritic cells induce antiviral CD8(+) T lymphocytes.

CD8(+) T cells are critical for the clearance of acute polyomavirus infection and the prevention of polyomavirus-induced tumors, but the antigen-presenting cell(s) involved in generating polyomavirus-specific CD8(+) T cells have not been defined. We investigated whether dendritic cells and macrophages are permissive for polyomavirus infection and examined their potential for inducing antiviral CD8(+) T cells. Although dendritic cells and macrophages both supported productive polyomavirus infection, dendritic cells were markedly more efficient at presenting the immunodominant viral epitope to CD8(+) T cells. Additionally, infected dendritic cells, but not infected macrophages, primed anti-polyomavirus CD8(+) T cells in vivo. Treatment with Flt3 ligand, a hematopoietic growth factor that dramatically expands the number of dendritic cells, markedly enhanced the magnitude of virus-specific CD8(+) T-cell responses during acute infection and the pool of memory anti-polyomavirus CD8(+) T cells. These findings suggest that virus-infected dendritic cells induce polyomavirus-specific CD8(+) T cells in vivo and raise the potential for their use as cellular adjuvants to promote CD8(+) T cell surveillance against polyomavirus-induced tumors.

3T3 Cells↗
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↗
PubMed2004

Polyomavirus infection in pediatric renal transplant recipients: evaluation using a quantitative real-time PCR technique.

Polyomavirus infection and related nephropathy is being increasingly recognized as an important cause of allograft dysfunction in adult renal transplant recipients. We prospectively monitored pediatric renal transplant recipients for the presence of BK and JC polyomavirus in urine and blood using a quantitative PCR assay to evaluate the prevalence and clinical relevance of polyomavirus infection in the pediatric renal transplant population. Of 46 pediatric renal recipients who were evaluated, nine (20%) demonstrated isolated BKV viruria, while five (11%) had concomitant BKV viremia and viruria. JCV viruria was found in eight (17%) patients. BKV viremia was associated with a significantly higher urinary BKV viral load: median urinary viral load 1.9 x 10(9) copies/mL (range 6.7 x 10(2)-1.8 x 10(11)) for the group with concomitant viremia and viruria vs. 1.8 x 10(3) copies/mL (range 2.5 x 10(2)-4.5 x 10(6)) for the group with isolated viruria (p < 0.0001). In children that were followed prospectively since their transplantation, the BKV urinary viral load increased markedly before viremia became detectable a few weeks later. None of the patients with JCV viruria or isolated BKV viruria had renal dysfunction. Among the five patients with BKV in both urine and blood, two developed biopsy-proven BKV nephropathy associated with deterioration of the renal function. Management of the BKV nephropathy consisted of reduction of immunosuppression alone or in combination with antiviral treatment with cidofovir. This study shows that polyomavirus infection and related interstitial nephritis is a relevant clinical issue in the pediatric renal transplant population. Monitoring the polyomaviral load in the urine and the blood of the patients using a quantitative PCR technique is a useful tool in the diagnosis and subsequent management of this infection. Even before viremia is present, an important rise in the urinary viral load should draw the attention of the transplant clinician and raise the issue of adapting the immunosuppression.

Adolescent↗
PubMed1991

Immunological elimination of infected cells as the candidate mechanism for tumor protection in polyomavirus-infected mice.

The uniformly lethal development of mammary tumors in polyomavirus-infected adult female nude mice was prevented by adoptive cell transfer of polyomavirus-immune splenocytes or peritoneal cells. Transferred immune cells also lowered the growth rate of emerging tumors. The induction of other relatively less frequent tumors of the skin and bone was decreased as well. Using in situ hybridization of whole-body sections as well as hybridization of nucleic acids from the mammary glands, we show for the first time that transferred immune cells, but not normal cells, virtually eliminated virus signal in the whole mouse and in the mammary glands. Since infected and tumorous mammary glands produce very little infectious virus, it appears that a major mechanism mediating the prevention of polyomavirus oncogenesis involves the immunological elimination of nonproductively and persistently infected cells.

Animals↗
PubMedDate not supplied

Use of immunocytochemistry on urinary sediments for the rapid identification of human polyomavirus infection. A case report.

The application of immunocytochemistry in urinary cytology for the identification of a human polyomavirus infection is described. The Papanicolaoustained slides of voided urine specimens of a 26-year-old man undergoing steroid therapy showed many inclusion-bearing epithelial cells. After subsequent destaining of the same slides, the presence of human papovavirus antigen in the nuclei of infected exfoliated cells was demonstrated by immunocytochemical staining with simian virus 40 antiserum and peroxidase. Papovaviruses were also detected by electron microscopic study of the smears, confirming the diagnosis of a human polyomavirus infection. The use of immunoperoxidase studies proved to be advantageous for the rapid cytodiagnosis of human polyomavirus infection in the urinary specimens in this case; such studies may be of particular value in equivocal cases to prove or disprove the viral nature of morphologic changes observed in routine preparations.

Adult↗
PubMed2002

Pathogenesis and management of polyomavirus infection in transplant recipients.

Polyomaviruses (JC virus [JCV], BK virus [BKV], and simian virus 40 [SV40]) establish subclinical and persistent infections and share the capacity for reactivation from latency in their host under immunosuppression. JCV establishes latency mainly in the kidney, and its reactivation results in the development of progressive multifocal leukoencephalopathy. BKV causes infection in the kidney and the urinary tract, and its activation causes a number of disorders, including nephropathy and hemorrhagic cystitis. Recent studies have reported SV40 in the allografts of children who received renal transplants and in the urine, blood, and kidneys of adults with focal segmental glomerulosclerosis, which is a cause of end-stage renal disease and an indication for kidney transplantation. Clinical syndromes related to polyomavirus infection are summarized in the present review, and strategies for the management of patients who receive transplants are discussed.

Cystitis↗
PubMedDate not supplied

Detection of avian polyomavirus infection by polymerase chain reaction using formalin-fixed, paraffin-embedded tissues.

Avian polyomavirus infection in psittacines was diagnosed in tissues by the use of polymerase chain reaction (PCR) test. The tissues used in the procedure were either formalin-fixed tissues embedded in paraffin blocks or fresh tissues (heart, liver, and spleen) collected from the psittacines during necropsy. DNA was extracted from these tissues and was tested with the published primers for avian polyomavirus VP1 gene in the PCR that yielded an amplicon of 550 base pair size, which was then visualized by electrophoresis. The amplicon size was consistent with avian polyomavirus. The PCR test was found to be an effective method for identifying avian polyomavirus infection in both formalin-fixed, paraffin-embedded and fresh tissues from psittacine birds of different age groups.

Animals↗
PubMed1998

Molecular biology and pathogenesis of human polyomavirus infections.

The two human polyomaviruses JC and BK are ubiquitous in the human population. Primary infection leads to lifelong persistence in the kidney, the CNS and in lymphoid cells. Virus is shed into the urine and is transmitted at least in part by the oral route. Under limited changes of the immunological state persistent polyomavirus infection is activated to an asymptomatic virus production. However, in severe long-lasting immunosuppression, highly effective virus multiplication can be accompanied by extended cytolytic damage of viral target cells leading to fatal disease. Whereas BKV is associated with severe urogenital disorders, JCV affects the CNS, leading to progressive multifocal leukoencephalopathy (PML). Although the number of PML cases is steadily increasing because of the AIDS epidemic, the mechanisms responsible for the change from asymptomatic-activated to the diseased state are not yet understood. As a possible pathogenic factor, the role of genomic heterogeneity of the transcriptional control region in the induction of disease is discussed.

BK Virus↗
PubMed2003

[Therapeutic possibilities for polyomavirus infections in renal transplantation].

TO IMPROVE THERAPEUTIC MANAGEMENT: The aim is the early detection of polyomavirus infection, before the onset of tubulo-interstitial nephritic lesions, and to reduce viral replication. AT THE STAGE OF POLYOMAVIRUS INFECTION: Treatment relies on the reduction of immunosuppression. Efficacy is controlled by monitoring the decoy cells in the urine and the detection and quantification of the DNA of polyomaviruses in the plasma and urine. AT THE STAGE OF POLYOMAVIRUS DISEASE: The aim is to reduce the viral replication by further decreasing immunosuppression to stabilize renal function and avoid graft rejection. When signs of rejection and viral infection co-exist, cidofovir could be a therapeutic alternative. However, the use of cidofovir remains in the field of clinical research and requires the further development of therapeutic protocols.

Antiviral Agents↗