Oxidative stress, a trigger of hepatitis C and B virus-induced liver carcinogenesis

Alexander V. Ivanov, Vladimir T. Valuev-Elliston, Daria A. Tyurina, Olga N. Ivanova, Sergey N. Kochetkov, Birke Bartosch, Maria G. Isaguliants

Research output: Contribution to journalArticlepeer-review

68 Citations (Scopus)

Abstract

Virally induced liver cancer usually evolves over long periods of time in the context of a strongly oxidative microenvironment, characterized by chronic liver inflammation and regeneration processes. They ultimately lead to oncogenic mutations in many cellular signaling cascades that drive cell growth and proliferation. Oxidative stress, induced by hepatitis viruses, therefore is one of the factors that drives the neoplastic transformation process in the liver. This review summarizes current knowledge on oxidative stress and oxidative stress responses induced by human hepatitis B and C viruses. It focuses on the molecular mechanisms by which these viruses activate cellular enzymes/systems that generate or scavenge reactive oxygen species (ROS) and control cellular redox homeostasis. The impact of an altered cellular redox homeostasis on the initiation and establishment of chronic viral infection, as well as on the course and outcome of liver fibrosis and hepatocarcinogenesis will be discussed The review neither discusses reactive nitrogen species, although their metabolism is interferes with that of ROS, nor antioxidants as potential therapeutic remedies against viral infections, both subjects meriting an independent review.

Original languageEnglish
Pages (from-to)3895-3932
Number of pages38
JournalOncotarget
Volume8
Issue number3
DOIs
Publication statusPublished - 2017

Keywords

  • Carcinogenesis
  • Hepatitis B virus
  • Hepatitis C virus
  • Pathogenesis
  • Reactive oxygen species

Field of Science

  • 3.2 Clinical medicine

Publication Type

  • 1.1. Scientific article indexed in Web of Science and/or Scopus database

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