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Beta HPV Deregulates Double-Strand Break Repair

Changkun Hu1, Nicholas Wallace1

  • 1Division of Biology, Kansas State University, Manhattan, KS 66506, USA.

Viruses
|May 28, 2022
PubMed

Insights

Beta human papillomavirus (beta HPV) infections may promote skin cancer by disrupting DNA repair. Beta HPV E6 protein impairs double-strand break repair, increasing UV mutagenesis in skin cells.

Area of Science:

  • Oncology
  • Virology
  • Genetics

Background:

  • Beta human papillomavirus (beta HPV) infections are prevalent in adults.
  • Certain beta HPV types are linked to nonmelanoma skin cancer (NMSC) in immunocompromised individuals.

Purpose of the Study:

  • To investigate if beta HPV infections contribute to NMSC in immunocompetent individuals.
  • To explore the mechanism by which beta HPV may increase genomic instability and UV mutagenesis.

Main Methods:

  • Utilized fluorescence-based reporters, next-generation sequencing, and animal models.
  • Focused on cells expressing beta HPV E6 and E7 proteins.
  • Examined the impact on DNA double-strand break (DSB) repair pathways.

Main Results:

  • Beta HPV E6 protein demonstrated a significant ability to increase UV mutagenesis.
  • Beta HPV E6 attenuates homologous recombination and non-homologous end-joining DSB repair pathways.
  • This dysregulation of DNA repair signaling is a key finding.

Conclusions:

  • Beta HPV E6 plays a role in impairing cellular DNA repair mechanisms.
  • This impairment may contribute to the development of NMSC, even in immunocompetent individuals.
  • Further research into these repair pathway disruptions is warranted.
Keywords:
Alt-EJDSB repairHRMMEJNHEJbeta HPV

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