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Viruses 2017, 9(11), 341;

Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle

Department of Anatomical and Cellular Pathology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, China
School of Biomedical Science, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China
Author to whom correspondence should be addressed.
Received: 15 September 2017 / Revised: 30 October 2017 / Accepted: 8 November 2017 / Published: 16 November 2017
(This article belongs to the Special Issue Viruses and the DNA Damage Response)
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The Epstein–Barr virus (EBV) is a ubiquitous virus that infects most of the human population. EBV infection is associated with multiple human cancers, including Burkitt’s lymphoma, Hodgkin’s lymphoma, a subset of gastric carcinomas, and almost all undifferentiated non-keratinizing nasopharyngeal carcinoma. Intensive research has shown that EBV triggers a DNA damage response (DDR) during primary infection and lytic reactivation. The EBV-encoded viral proteins have been implicated in deregulating the DDR signaling pathways. The consequences of DDR inactivation lead to genomic instability and promote cellular transformation. This review summarizes the current understanding of the relationship between EBV infection and the DDR transducers, including ATM (ataxia telangiectasia mutated), ATR (ATM and Rad3-related), and DNA-PK (DNA-dependent protein kinase), and discusses how EBV manipulates the DDR signaling pathways to complete the replication process of viral DNA during lytic reactivation. View Full-Text
Keywords: Epstein–Barr virus; DNA damage response; lytic reactivation Epstein–Barr virus; DNA damage response; lytic reactivation

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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. (CC BY 4.0).

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Hau, P.M.; Tsao, S.W. Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle. Viruses 2017, 9, 341.

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