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Oxidative Medicine and Cellular Longevity
Volume 2017, Article ID 3179421, 16 pages
Review Article

DNA Oncogenic Virus-Induced Oxidative Stress, Genomic Damage, and Aberrant Epigenetic Alterations

1Division of Hepatology, Department of Medicine, Faculty of Health Sciences, Groote Schuur Hospital, University of Cape Town, Cape Town, South Africa
2Division of Rheumatology, Department of Medicine, Faculty of Health Sciences, Groote Schuur Hospital, Cape Town, South Africa

Correspondence should be addressed to Mankgopo Magdeline Kgatle; moc.liamg@eltagk.opogknam

Received 27 January 2017; Revised 1 May 2017; Accepted 23 May 2017; Published 27 June 2017

Academic Editor: Peeter Karihtala

Copyright © 2017 Mankgopo Magdeline Kgatle et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Approximately 20% of human cancers is attributable to DNA oncogenic viruses such as human papillomavirus (HPV), hepatitis B virus (HBV), and Epstein-Barr virus (EBV). Unrepaired DNA damage is the most common and overlapping feature of these DNA oncogenic viruses and a source of genomic instability and tumour development. Sustained DNA damage results from unceasing production of reactive oxygen species and activation of inflammasome cascades that trigger genomic changes and increased propensity of epigenetic alterations. Accumulation of epigenetic alterations may interfere with genome-wide cellular signalling machineries and promote malignant transformation leading to cancer development. Untangling and understanding the underlying mechanisms that promote these detrimental effects remain the major objectives for ongoing research and hope for effective virus-induced cancer therapy. Here, we review current literature with an emphasis on how DNA damage influences HPV, HVB, and EBV replication and epigenetic alterations that are associated with carcinogenesis.