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Measurement of BK-polyomavirus Non-Coding Control Region Driven Transcriptional Activity Via Flow Cytometry

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Tumor Necrosis Factor-Alpha Inhibits the Replication of Patient-Derived Archetype BK Polyomavirus While Activating

Lise Lauterbach-Rivière¹, Lucia Thuringer^1,2, Pascal Feld¹

¹Institute of Virology, Saarland University Medical Center, Homburg, Germany.

Journal of Medical Virology

|February 14, 2025

Summary

Tumor necrosis factor-alpha (TNF-α) impacts BK polyomavirus (BKPyV) differently based on its genetic type. TNF-α enhances rearranged BKPyV replication but suppresses archetype BKPyV, affecting kidney transplant outcomes.

Keywords:

BK polyomavirus (BKPyV)IFN‐γ TNF‐α antiviral therapy archetype drug discovery non‐coding control region (NCCR)

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Area of Science:

Virology
Immunology
Nephrology

Background:

BK polyomavirus (BKPyV) reactivation causes significant nephropathy in kidney transplant recipients.
No approved drugs exist for BKPyV reactivation.
Tumor necrosis factor-alpha (TNF-α) blockade is a potential therapy, but its effect on BKPyV archetypes is unknown.

Purpose of the Study:

To investigate the effect of TNF-α on different BKPyV archetypes.
To understand the mechanisms underlying TNF-α's influence on BKPyV replication.
To establish a reliable assay for testing BKPyV therapies.

Main Methods:

Optimized cell culture for robust replication of wild-type (ww) BKPyV.
Utilized primary renal proximal tubule epithelial cells (RPTEC) and patient-derived BKPyV strains.
Employed siRNAs, chimeric, and mutated BKPyV strains for mechanistic analysis.

Main Results:

TNF-α promoted replication of rearranged (rr) BKPyV but suppressed wild-type (ww) BKPyV.
Interferon-gamma (IFN-γ) suppressed BKPyV replication, even with TNF-α present.
TNF-α's effect on rr-BKPyV replication is mediated by the NF-κB p65 pathway, not the conserved NF-κB binding site.

Conclusions:

TNF-α blockade might hinder natural anti-BKPyV control in transplant patients with archetype infections.
Impaired T_H1 responses could make TNF-α blockade detrimental.
Inflammation may select for BKPyV variants resistant to TNF-α suppression, highlighting the need for clinically relevant BKPyV isolates in drug discovery.