Viruses and the host replisome: discovering oncogenic mechanisms of small DNA tumor viruses

Christopher D Collins1,2,3, Matthew Stefely2, Kavi Prem Milan Mehta4

  • 1John W. and Jeanne M. Rowe Center for Research in Virology, Madison, Wisconsin, USA.

Journal of Virology
|January 7, 2026
PubMed

Insights

Human papillomavirus (HPV) and Merkel cell polyomavirus (MCPyV) oncoproteins disrupt the host replisome, leading to genomic instability and cancer. New technologies like iPOND help uncover these viral mechanisms for better understanding of oncogenesis.

Area of Science:

  • Oncogenic viruses
  • Genomic instability
  • DNA replication

Background:

  • Human papillomavirus (HPV) and Merkel cell polyomavirus (MCPyV) are DNA tumor viruses implicated in human cancers.
  • The precise mechanisms by which viral oncoproteins induce genomic instability remain incompletely understood.

Purpose of the Study:

  • To review the influence of HPV and MCPyV oncoproteins on the host replisome.
  • To highlight the role of emerging technologies in studying viral oncogenesis.

Main Methods:

  • Literature review of studies on viral oncoproteins and host DNA replication.
  • Discussion of advanced techniques such as isolation of proteins on nascent DNA (iPOND).

Main Results:

  • Viral oncoproteins interact with and dysregulate components of the host replisome.
  • These disruptions contribute to the genomic instability observed in virus-associated cancers.

Conclusions:

  • Understanding the interplay between viral oncoproteins and the host replisome is crucial for deciphering viral oncogenesis.
  • Technologies like iPOND offer powerful tools for future discoveries in this field.

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