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Viruses 2017, 9(8), 232;

Human Papillomavirus and the DNA Damage Response: Exploiting Host Repair Pathways for Viral Replication

Department of Microbiology-Immunology, Northwestern University, Feinberg School of Medicine, 303 E. Chicago Ave., Chicago, IL 60611, USA
Author to whom correspondence should be addressed.
Academic Editor: Micah Luftig
Received: 22 June 2017 / Revised: 11 August 2017 / Accepted: 14 August 2017 / Published: 18 August 2017
(This article belongs to the Special Issue Viruses and the DNA Damage Response)
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High-risk human papillomaviruses (HPVs) are the causative agents of cervical and other genital cancers. In addition, HPV infections are associated with the development of many oropharyngeal cancers. HPVs activate and repress a number of host cellular pathways to promote their viral life cycles, including those of the DNA damage response. High-risk HPVs activate the ataxia telangiectasia-mutated (ATM) and ATM and Rad3-related (ATR) DNA damage repair pathways, which are essential for viral replication (particularly differentiation-dependent genome amplification). These DNA repair pathways are critical in maintaining host genomic integrity and stability and are often dysregulated or mutated in human cancers. Understanding how these pathways contribute to HPV replication and transformation may lead to the identification of new therapeutic targets for the treatment of existing HPV infections. View Full-Text
Keywords: human papillomavirus; DNA damage response; replication human papillomavirus; DNA damage response; replication

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Spriggs, C.C.; Laimins, L.A. Human Papillomavirus and the DNA Damage Response: Exploiting Host Repair Pathways for Viral Replication. Viruses 2017, 9, 232.

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