ArticleViruses2022
Polyomavirus BK Genome Comparison Shows High Genetic Diversity in Kidney Transplant Recipients Three Months after Transplantation.
Article in Viruses, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
- Interferon-Inducible Gene Upregulation Correlates With Successful Viral Clearance in Patients With BK Polyomavirus-Associated Nephropathy.Kidney international reports · 2026Article
- The Burden of BK Polyomavirus in Pediatric Renal Transplantation: A Belgian Experience.Biomedicines · 2026Article
- Case Report: Late-onset BK polyomavirus-associated nephropathy in kidney transplant recipients: two cases and insights into underlying mechanisms.Frontiers in medicine · 2026Review
- Donor HLA-DQ genetic and functional divergence affect the control of BK polyoma virus infection after kidney transplantation.Science advances · 2025Article
- [Clinical presentation and treatment of herpes zoster and postherpetic neuralgia].Dermatologie (Heidelberg, Germany) · 2024Review
- BK Polyomavirus in Pediatric Renal Transplantation-What We Know and What We Do Not.Biomedicines · 2024Review
- Time-dependent variations in BK polyomavirus genome from kidney transplant recipients with persistent viremia.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
8 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 generally divided into twelve subgroups based on the genetic diversity of Viral Protein 1 (VP1). BKPyV can cause polyomavirus-associated nephropathy (PVAN) after kidney transplantation. Detection of BKPyV DNA in blood (viremia) is a source of concern and increase in plasma viral load is associated with a higher risk of developing PVAN. In this work, we looked for possible associations of specific BKPyV genetic features with higher plasma viral load in kidney transplant patients. We analyzed BKPyV complete genome in three-month samples from kidney recipients who developed viremia during their follow-up period. BKPyV sequences were obtained by next-generation sequencing and were de novo assembled using the new BKAnaLite pipeline. Based on the data from 72 patients, we identified 24 viral groups with unique amino acid sequences: three in the VP1 subgroup IVc2, six in Ib1, ten in Ib2, one in Ia, and four in II. In none of the groups did the mean plasma viral load reach a statistically significant difference from the overall mean observed at three months after transplantation. Further investigation is needed to better understand the link between the newly described BKPyV genetic variants and pathogenicity in kidney transplant recipients.
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