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Updated: Sep 27, 2025

Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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BK Polyomavirus Requires the Mismatch Repair Pathway for DNA Damage Response Activation.

Joshua L Justice1, Jason M Needham1, Brandy Verhalen1

  • 1Department of Microbiology, University of Alabama at Birminghamgrid.265892.2, Birmingham, Alabama, USA.

Journal of Virology
|April 7, 2022
PubMed
Summary

The mismatch repair pathway is crucial for activating the DNA damage response during BK polyomavirus (PyV) infection. This pathway

Keywords:
BK polyomavirusDNA damage responseMSH6mismatch repair

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Area of Science:

  • Virology and Molecular Biology
  • Immunology and Infectious Diseases

Background:

  • BK polyomavirus (PyV) reactivation is a major cause of graft failure in kidney transplant recipients.
  • PyV manipulates host cell machinery, including the DNA damage response (DDR), for replication.
  • The precise mechanism by which PyV activates the DDR remains uncharacterized.

Purpose of the Study:

  • To investigate the role of the mismatch repair (MMR) pathway in BKPyV-induced DDR activation.
  • To elucidate the impact of MMR pathway disruption on viral replication and assembly.

Main Methods:

  • Silencing of Msh6, a component of the MutSα MMR complex, in BKPyV-infected primary cells.
  • Assessment of DNA damage, DDR activation, and cell cycle progression.
  • Quantification of infectious viral particles and viral protein levels (VP2).

Main Results:

  • Msh6 silencing led to severe DNA damage and impaired DDR activation, causing cell cycle dysregulation.
  • Reduced Msh6 expression significantly decreased infectious viral particle production.
  • Fewer infectious virions were observed due to lower levels of the minor capsid protein VP2.

Conclusions:

  • The MMR pathway is essential for effective DDR activation during BKPyV infection.
  • MMR pathway integrity is required for optimal viral replication and assembly, potentially by maintaining nuclear integrity.
  • Targeting the DDR pathway may offer a therapeutic strategy to reduce BKPyV viral loads by affecting virion assembly.