Functional implications of mitochondrial reactive oxygen species generated by oncogenic viruses

Young Bong Choi1, Edward William Harhaj1

  • 1Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns HopkinsSchool of Medicine, Baltimore, MD 21287, USA.

Frontiers in Biology
|January 13, 2015
PubMed

Insights

Oncogenic viruses hijack mitochondria, impacting cell survival and promoting cancer. This review explores how viruses manipulate mitophagy and metabolism for oncogenesis.

Area of Science:

  • Virology
  • Cell Biology
  • Cancer Research

Background:

  • 15-20% of human cancers are linked to oncogenic viral infections.
  • Oncogenic viruses like HPV, HBV, HCV, and HTLV-1 exploit host cell mitochondria.
  • Viral infections can induce oxidative stress and DNA damage, contributing to cancer development.

Purpose of the Study:

  • To review recent advancements in understanding viral regulation of mitochondria.
  • To explore the role of mitophagy and metabolic adaptation in viral oncogenesis.
  • To highlight how viral oncogenes subvert cellular quality control and metabolic pathways.

Main Methods:

  • Literature review of studies on oncogenic viruses and mitochondrial function.
  • Analysis of research on viral manipulation of mitophagy and metabolic pathways.
  • Synthesis of findings on the link between viral-induced mitochondrial changes and cancer.

Main Results:

  • Oncogenic viruses target mitochondria to control cell proliferation and survival.
  • Viral gene products induce reactive oxygen species, causing DNA damage and activating oncogenic signaling.
  • Viruses subvert mitophagy and metabolic adaptation to facilitate their replication and promote cancer.

Conclusions:

  • Mitochondrial regulation by oncogenic viruses is a critical factor in viral oncogenesis.
  • Understanding viral manipulation of mitophagy and metabolism offers potential therapeutic targets.
  • Further research into these mechanisms is crucial for developing anti-cancer strategies.

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