ArticleScientific reports2023
Time-dependent variations in BK polyomavirus genome from kidney transplant recipients with persistent viremia.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- Urinary VP1 Flow Cytometry as a Complementary Approach for BK Polyomavirus Monitoring: A Proof-Of-Concept Study.Transplant international : official journal of the European Society for Organ Transplantation · 2026Observational
- Case Report: Late-onset BK polyomavirus-associated nephropathy in kidney transplant recipients: two cases and insights into underlying mechanisms.Frontiers in medicine · 2026Review
- Establishment of a Stable BK Polyomavirus-Secreting Cell Line: Characterization of Viral Genome Integration and Replication Dynamics Through Comprehensive Analysis.International journal of molecular sciences · 2025Article
- Review
- Imidazopyrimidine: from a relatively exotic scaffold to an evolving structural motif in drug discovery.RSC medicinal chemistry · 2024Review
- Acute Kidney Injury and BK Polyomavirus in Urine Sediment Cells.International journal of molecular sciences · 2023Article
- Prevalence of IgG antibodies against Malawi polyomavirus in patients with autoimmune diseases and lymphoproliferative disorders subjected to bone marrow transplantation.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BK polyomavirus (BKPyV) is a human DNA virus that resides latent in the host's renal tissue. Reactivation occurs occasionally and in case of kidney transplantation, it can lead to polyomavirus-associated nephropathy (PVAN). Due to the lack of specific antivirals for BKPyV and despite the risk of allograft rejection, reduction of immunosuppression remains the main approach for treating PVAN. Current data suggests that mutations can accumulate over time in the major capsid protein VP1 and can lead to neutralization escape in kidney transplant recipients. Herein, we show that mutations occur throughout the entire BKPyV genome, including in VP1. Changes were identified by per-patient comparison of viral genome sequences obtained in samples from 32 kidney recipients with persistent viremia collected at different post-transplant time-points. Amino acid changes were observed in both earlier and later post-transplant samples, although some of them were only found in later samples. Changes in VP1 mainly consisted in the introduction of a new amino acid. A switch back to the conservative amino acid was also observed. This should be considered in future approaches for treating BKPyV infection in kidney transplant recipients.
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Registered trials
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