ArticleJournal of cellular physiology2010
Mutations in the external loops of BK virus VP1 and urine viral load in renal transplant recipients.
Article in Journal of cellular physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- Live long and persist: polyomavirus immune evasion in the brain and kidney.Future virology · 2025Article
- The role of the DE and EF loop of BKPyV VP1 in the serological cross-reactivity between subtypes.Virus research · 2023Article
- Article
- Stepwise Reduction of Mycophenolate Mofetil with Conversion to Everolimus for the Treatment of Active BKV in Kidney Transplant Recipients: A Single-Center Experience in Vietnam.Journal of clinical medicine · 2022Article
- T cell deficiency precipitates antibody evasion and emergence of neurovirulent polyomavirus.eLife · 2022Article
- Molecular characterization of BK virus detected in renal transplant patients in Sri Lanka: a preliminary study.The Indian journal of medical research · 2022Article
- Genomic Mutations of BK Polyomavirus in Patients after Kidney Transplantation: A Cross-Sectional Study in Vietnam.Journal of clinical medicine · 2022Article
- Translating genomic exploration of the familyiScience · 2022Article
- JCPyV VP1 Mutations in Progressive MultifocalLeukoencephalopathy: Altering Tropismor Mediating Immune Evasion?Viruses · 2020Review
- Persistent BK Polyomavirus Viruria is Associated with Accumulation of VP1 Mutations and Neutralization Escape.Viruses · 2020Article
- Intra-patient viral evolution in polyomavirus-related diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- Article
- Characterization of BK Polyomaviruses from Kidney Transplant Recipients Suggests a Role for APOBEC3 in Driving In-Host Virus Evolution.Cell host & microbe · 2018Article
- Molecular characterization of BK virus in patients infected with human immunodeficiency virus.Medical microbiology and immunology · 2016Article
- Early identification of renal transplant recipients with high risk of polyomavirus-associated nephropathy.Medical microbiology and immunology · 2015Article
- JC virus urinary excretion and seroprevalence in natalizumab-treated multiple sclerosis patients.Journal of neurovirology · 2015Article
- Limited Variation in BK Virus T-Cell Epitopes Revealed by Next-Generation Sequencing.Journal of clinical microbiology · 2015Article
- Evidence supporting the association of polyomavirus BK genome with prostate cancer.Medical microbiology and immunology · 2013Article
- Detection of BK virus in urine from renal transplant subjects by mass spectrometry.Clinical proteomics · 2012Article
- Management of polyomavirus-associated nephropathy in renal transplant recipients.Nature reviews. Nephrology · 2012Review
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Polyomavirus-associated nephropathy (PVAN) is a major complication that occurs after renal transplantation and is induced by reactivation of the human polyomavirus BK (BKV). The structure of the viral capsid protein 1 (VP1) is characterized by the presence of external loops, BC, DE, EF, GH, and HI, which are involved in receptor binding. The pathogenesis of PVAN is not well understood, but viral risk factors are thought to play a crucial role in the onset of this pathology. In an attempt to better understand PVAN pathogenesis, the BKV-VP1 coding region was amplified, cloned, and sequenced from the urine of kidney transplant recipients who did, and did not, develop the pathology. Urine viral loads were determined by using real time quantitative PCR (Q-PCR). Amino acid substitutions were detected in 6/8 patients, and 6/7 controls. The BC and EF loop regions were most frequently affected by mutations, while no mutations were found within the GH and HI loops of both patients and controls. Some mutations, that were exclusively detected in the urine of PVAN patients, overlapped with previously reported mutations, although a correlation between changes in amino acids and the development of PVAN was not found. Urine viral loads were higher than that of the proposed cut-off loads for identification of patients that are at a high risk of developing PVAN (10(7) copies/ml), both in the PVAN and control groups, thus confirming that urine viral load is not a useful predictive marker for the development of PVAN.
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