JC polyomavirus nephropathy confirmed by using an in‐house polymerase chain reaction method

Querido, Sara; Jorge, Cristina; Sousa, Henrique; Birne, Rita; Matias, Patrícia; Weigert, André; Adragão, Teresa; Bruges, Margarida; Ramos, Sância; Santos, Madalena; Paixão, Paulo; Curran, Martin D.; Machado, Domingos

doi:10.1111/tid.12426

Cited by 7 publications

(13 citation statements)

References 26 publications

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“…Indeed, kidney transplant patients are at risk of premature allograft failure (Castro et al, ; Funahashi et al, ). At risk patients can be identified before significant functional impairment of the renal allograft occurs (Castro et al, ; Chan et al, ; Funahashi et al, ; Querido et al, ; Saundh, Baker, Harris, & Hale, ). Our innovative ELISA with JCPyV VP1 mimotopes will be useful to study multiple sclerosis (MS) affected patients treated with monoclonal antibodies (mab), such as the natalizumab (Reuwer, Heron, van der Dussen, Schneider‐Hohendorf, & Murk, ).…”

Section: Discussionmentioning

confidence: 99%

Serum IgG antibodies from healthy subjects up to 100 years old react to JC polyomavirus

Bononi

Mazzoni

Pietrobon

et al. 2018

Journal Cellular Physiology

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JC polyomavirus (JCPyV) was identified in 1971 in the brain tissue of a patient (J.C.) affected by the progressive multifocal leukoencephalopathy (PML). JCPyV encodes for the oncoproteins large T antigen (Tag) and small t-antigen (tag). These oncoproteins are responsible of the cell transformation and tumorigenesis in experimental animals. JCPyV is ubiquitous in human populations. After the primary infection, which is usually asymptomatic, JCPyV remains lifelong in the host in a latent phase. Its reactivation may occur in heathy subjects and immunocompromised patients. Upon reactivation, JCPyV could reach (i) the CNS inducing the PML, (ii) the kidney of transplant patients causing the organ rejection. Association between JCPyV, which is a small DNA tumor virus, and gliomas and colorectal carcinomas has been published. In the present investigation, we report on a new indirect ELISA with two specific synthetic peptides mimicking JCPyV VP1 immunogenic epitopes to detect specific serum IgG antibodies against JCPyV. Serum samples of healthy subjects (n = 355) ranging 2-100 years old, were analyzed by this new indirect ELISA. The linear peptides VP1 K and VP1 N resemble the natural JCPyV VP1 capsidic epitopes constituting a docking site for serum antibodies. Data from this innovative immunologic assay indicate that the overall prevalence of JCPyV-VP1 antibodies in healthy subjects is at 39%. The innovative indirect ELISA with JCPyV VP1 mimotopes seems to be a useful method to detect specific IgG antibodies against this virus, without cross-reactivity with the closely related SV40 and BKPyV polyomaviruses.

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Section: Discussionmentioning

confidence: 99%

Serum IgG antibodies from healthy subjects up to 100 years old react to JC polyomavirus

Bononi

Mazzoni

Pietrobon

et al. 2018

Journal Cellular Physiology

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“…Tubular epithelial nuclei stained positive for anti‐simian virus 40 (SV40) antigen by immunohistochemistry, which detects large T antigen (LTag) of all human polyomavirus. In addition, specific in‐house real‐time qPCR assay confirmed JCV DNA and excluded BKV DNA in paraffin‐embedded allograft tissue …”

Section: Case Reportmentioning

confidence: 99%

High-grade urothelial carcinoma in a kidney transplant recipient after JC virus nephropathy: The first evidence of JC virus as a potential oncovirus in bladder cancer

Querido

Fernandes

Weigert

et al. 2020

American Journal of Transplantation

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Kidney transplant (KT) recipients have an increased risk for urothelial carcinoma. A role for JC virus (JCV) in human cancers is not yet proved but there is an increasingly reported association between BK virus (BKV) nephropathy and renourinary neoplasms. We report a KT recipient who developed a high‐grade urothelial carcinoma 5 years after a diagnosis of JCV nephropathy and 9 years after kidney transplantation. Neoplastic tissue was positive for JCV DNA by real‐time polymerase chain reaction (PCR). Immunochemical staining showed strong positivity for cell cycle markers (p16, p53, and Ki67) and for early viral protein JCV large T antigen (JCV LTag; using a broad polyomavirus antibody); however, late viral protein (VP1) stained negative. In contrast, in non‐neoplastic urothelium, JCV DNA and all immunochemical markers were negative. These facts suggest that malignancy was induced by JCV. To the best of our knowledge, this is the first report of urothelial high‐grade carcinoma associated with JCV nephropathy in a KT recipient.

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“…Incidence of polyomavirus‐associated nephropathy (PVAN) secondary to BKPyV varies from 1% to 10% of kidney transplant patients and of these, 30%‐80% of the cases develop allograft failure at the late stage of disease . On the other hand, JCPyVAN accounts for only 0.9%‐3% of PVAN cases . This difference could be explained partly by the fact that BKPyV viruria has been documented more often compared to JCPyV viruria (36% vs 28%) in kidney transplant recipients, while concomitant infection has been found in 11% of kidney transplant patients …”

Section: Introductionmentioning

confidence: 99%

“…Frequently, primary polyomavirus infections have not been associated with any clinical syndromes . In the presence of anti T‐cell agents necessary for organ transplant patients, immune status can be weakened, viral reactivation becomes more prominent and possibly causes PML, particularly from JCPyV, and genitourinary tract injury to a lesser extent .…”

Section: Introductionmentioning

confidence: 99%

“…In the presence of anti T‐cell agents necessary for organ transplant patients, immune status can be weakened, viral reactivation becomes more prominent and possibly causes PML, particularly from JCPyV, and genitourinary tract injury to a lesser extent . Damage to the genitourinary tract secondary to such viruses may lead to allograft dysfunction in renal transplant patients especially during the first 2 years after transplantation; however, this dysfunction seems uncommon with JCPyV . Only one case thus far has been reported of early allograft dysfunction due to JCPyVAN at 6 months post transplant .…”

Section: Introductionmentioning

confidence: 99%

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Absence of JC polyomavirus (JCPyV) viremia in early post‐transplant JCPyV nephropathy: A case report

Janphram

Worawichawong

Disthabanchong

et al. 2017

Transplant Infectious Dis

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JC polyomavirus (JCPyV)-associated nephropathy (JCPyVAN) occurs in <3% of PVAN cases after renal transplantation. We report the first confirmed case to our knowledge of JCPyVAN diagnosed by kidney biopsy in the early 6 months post transplant in Thailand. In this case report, recovery of renal allograft function was not observed after reduction of immunosuppressive agents and administration of intravenous immunoglobulin and cidofovir. Despite persistent JCPyV viruria, no significant further decline in allograft function was documented at 15 months post transplant. K E Y W O R D Sallograft dysfunction, JC virus nephropathy, kidney transplant

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JC polyomavirus nephropathy confirmed by using an in‐house polymerase chain reaction method

Cited by 7 publications

References 26 publications

Serum IgG antibodies from healthy subjects up to 100 years old react to JC polyomavirus

Serum IgG antibodies from healthy subjects up to 100 years old react to JC polyomavirus

High-grade urothelial carcinoma in a kidney transplant recipient after JC virus nephropathy: The first evidence of JC virus as a potential oncovirus in bladder cancer

Absence of JC polyomavirus (JCPyV) viremia in early post‐transplant JCPyV nephropathy: A case report

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