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Related Experiment Video

Updated: Jun 11, 2026

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

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Published on: November 7, 2017

A Mouse Model for "Definitive" Polyomavirus Nephropathy with End-Organ Injury.

Volker Nickeleit¹, Dalton Butcher¹, Bawana Thompson¹

¹Department of Pathology and Laboratory Medicine, Division of Nephropathology, The University of North Carolina School of Medicine (UNC-SOM), Brinkhous-Bullitt Building, CB# 7525, Chapel Hill, NC 27599, USA.

|February 27, 2026

Summary

This summary is machine-generated.

Researchers developed a new mouse model for polyomavirus nephropathy (PyVN), a kidney disease caused by polyomavirus. This model accurately mimics human PyVN, aiding research into its causes and potential treatments.

Keywords:

BK-Polyomavirus histology lytic viral replication mouse model nephropathy tubular injury urinary Haufen

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Area of Science:

Virology
Nephrology
Immunology

Background:

Polyomavirus nephropathy (PyVN) is a significant cause of kidney disease in humans.
Existing mouse models do not fully replicate the lytic viral replication and end-organ damage seen in human PyVN.

Purpose of the Study:

To establish a reliable mouse model for studying polyomavirus nephropathy (PyVN).
To investigate the pathogenesis of PyVN, including viral replication, tubular injury, and immune responses.
To provide a platform for testing therapeutic interventions against PyVN.

Main Methods:

Newborn Black-Swiss mice were inoculated with murine polyomavirus (MuPyV).
Comprehensive analyses included morphological, immunohistochemical, molecular, genetic, and immunological assessments.
Long-term monitoring tracked viral dynamics, kidney pathology, and immune responses over 54 weeks.

Main Results:

The model demonstrated productive intrarenal MuPyV infection with acute tubular injury and lytic replication.
High viral loads and gene expression were observed, followed by viral clearance and minimal residual infection.
A robust IgM/IgG immune response was induced, and the virus remained genetically stable throughout the infection.

Conclusions:

The developed mouse model accurately recapitulates human polyomavirus nephropathy (PyVN).
This model is suitable for research on PyVN pathogenesis, viral-induced tubular injury, and host-pathogen immune interactions.
It serves as a valuable tool for in vivo evaluation of novel therapeutic strategies targeting PyVN.