Ubiquitination at the interface of tumor viruses and DNA damage responses

Joseph M Dybas1, Christin Herrmann2, Matthew D Weitzman3

  • 1Division of Protective Immunity and Division of Cancer Pathobiology, Children's Hospital of Philadelphia, Philadelphia, PA, USA; Department of Biomedical and Health Informatics, Children's Hospital of Philadelphia, Philadelphia, PA, USA.

Current Opinion in Virology
|September 28, 2018
PubMed

Insights

Viruses hijack the cell's ubiquitination system to alter the DNA damage response (DDR), impacting viral replication and potentially causing cancer. This review explores how viruses manipulate DDR pathways for their benefit.

Area of Science:

  • Virology
  • Molecular Biology
  • Cellular Biology

Background:

  • Viruses manipulate host cell machinery for replication.
  • Ubiquitination is a key cellular process regulating protein function and degradation.
  • The DNA damage response (DDR) is crucial for maintaining genomic stability.

Purpose of the Study:

  • To review how viruses exploit the cellular ubiquitination system.
  • To understand the manipulation of the DNA damage response (DDR) by viruses.
  • To explore the link between viral manipulation of DDR and host cellular transformation.

Main Methods:

  • Literature review of viral hijacking of ubiquitination.
  • Analysis of host-pathogen interactions involving DDR pathways.
  • Examination of the role of ubiquitination in viral replication and oncogenesis.

Main Results:

  • Viruses utilize ubiquitination to modulate host proteostasis and promote infection.
  • Viral manipulation of DDR pathways can enhance viral replication.
  • Altered DDR by viruses contributes to genomic instability and cellular transformation.

Conclusions:

  • Viruses extensively co-opt the ubiquitination machinery to subvert host DDR pathways.
  • Understanding these interactions is critical for developing antiviral strategies and cancer therapies.
  • Targeting viral manipulation of ubiquitination offers potential therapeutic avenues.

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