Polyomavirus

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 1236

Special Issue Editors


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Guest Editor
Department of Microbiology, The University of Alabama at Birmingham, Birmingham, AL 35205, USA
Interests: cell cycle control during BK polyomavirus infection; DNA damage response during BK polyomavirus infection; BK polyomavirus reactivation following kidney transplant; single-cell virology

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Guest Editor
Department of Molecular Genetics and Biochemistry, The University of Pittsburgh, Pittsburgh, PA 15213, USA
Interests: oncogenic viruses; Merkel cell polyomavirus; circular RNAs; vaccines

Special Issue Information

Dear Colleagues,

Polyomaviruses are small, non-enveloped, double-stranded DNA viruses that cause lifelong persistent infection without clinical symptoms in healthy people but can result in significant morbidity and mortality in immunocompromised individuals. Understanding how these viruses are transmitted, how their genomes are maintained in various cell types, and how their reactivation can cause pathogenesis and/or cancer has been the subject of rigorous study for decades. The size of this virus makes it dependent upon host pathways, and its lifelong persistence suggests immune evasion mechanisms.

Human polyomaviruses such as BK and JC are associated with serious diseases in immunocompromised individuals such as polyomavirus nephropathy, hemorrhagic cystitis, and progressive multifocal leukoencephalopathy. Merkel cell polyomavirus can cause Merkel cell carcinomas in elderly patients.

This Special Issue, titled “Polyomavirus”, will provide the most up-to-date insights into virus–host interactions, pathology, phylogeny, immune response, and structure function relationships for Simian virus 40, BK polyomaviruses, JC polyomaviruses, Merkel cell polyomaviruses, and murine polyomavirus, as well as newly discovered polyomaviruses. Scientists worldwide are welcome to contribute original research papers, brief reports, technical notes, and reviews to share current models in the field. We aim to cover both recent and historical advances in the field of polyomavirus DNA tumor viruses.

Dr. Sunnie R. Thompson
Prof. Dr. Patrick S. Moore
Guest Editors

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Keywords

  • virus–host interactions
  • viral life cycle
  • viral replication
  • pathogenesis
  • phylogeny
  • structure
  • transcription
  • packaging
  • trafficking
  • persistence
  • re-arrangements
  • gene regulation
  • reactivation
  • miRNA
  • viral immune evasion
  • vaccines

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Published Papers (1 paper)

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Research

30 pages, 3776 KB  
Article
Divergent Fates of Kidney-Resident Polyomaviruses: Stable Shedding Versus Near-Silent Persistence
by Anik Mojumder, Kimin W. Nguyen and Christopher S. Sullivan
Viruses 2026, 18(3), 359; https://doi.org/10.3390/v18030359 - 15 Mar 2026
Viewed by 796
Abstract
Polyomaviruses establish long-term infection in the kidney and are intermittently shed in urine. However, the relationship between kidney-resident viral genomes and urinary shedding during persistent infection remains poorly defined. Using a genetically barcoded murine polyomavirus library, we tracked thousands of viral lineages in [...] Read more.
Polyomaviruses establish long-term infection in the kidney and are intermittently shed in urine. However, the relationship between kidney-resident viral genomes and urinary shedding during persistent infection remains poorly defined. Using a genetically barcoded murine polyomavirus library, we tracked thousands of viral lineages in vivo by pairing longitudinal urine sampling with endpoint barcode sequencing of kidney tissue in four mice. Across all animals, kidney infection consistently resolved into two stable viral populations, with near-silent persistence as the dominant fate. Most kidney-resident barcodes were never detected in late urine at late stages of infection, even though many reached substantial abundance within the kidney, demonstrating that kidney viral genome levels alone do not predict urinary shedding. In contrast, only a small minority of kidney barcodes contributed disproportionately to urine virus output at late timepoints, and these barcodes exhibited stable longitudinal behavior, with repeated detection in urine over time and markedly higher peak urine abundance than late non-shed or random barcode controls. Shedding behavior was not explained by input virus stock abundance, barcode sequence features, predicted miRNA targeting, or ongoing reseeding from blood or other tissues. Instead, barcodes that ultimately dominated late urine already showed elevated urine detection early after infection, indicating that shedding fate is established early and maintained throughout persistent infection. Together, these findings reveal that persistent kidney infection is a structured reservoir composed of a large population of deeply restricted viral genomes and a smaller, stable subset that repeatedly produces urine-detectable viruses, with concurrent smoldering infections and latency-like restriction representing one possible model to explain the sharply different probabilities of shedding among kidney-resident genomes. Full article
(This article belongs to the Special Issue Polyomavirus)
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