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

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 car...

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Main Authors: Pok Man Hau, Sai Wah Tsao
Format: Article
Language:English
Published: MDPI AG 2017-11-01
Series:Viruses
Subjects:
Online Access:https://www.mdpi.com/1999-4915/9/11/341
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spelling doaj-0a496371f07f4860a7e68cacbd6388c22020-11-25T00:07:27ZengMDPI AGViruses1999-49152017-11-0191134110.3390/v9110341v9110341Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life CyclePok Man Hau0Sai Wah Tsao1Department of Anatomical and Cellular Pathology, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, ChinaSchool of Biomedical Science, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, ChinaThe 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.https://www.mdpi.com/1999-4915/9/11/341Epstein–Barr virusDNA damage responselytic reactivation
collection DOAJ
language English
format Article
sources DOAJ
author Pok Man Hau
Sai Wah Tsao
spellingShingle Pok Man Hau
Sai Wah Tsao
Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle
Viruses
Epstein–Barr virus
DNA damage response
lytic reactivation
author_facet Pok Man Hau
Sai Wah Tsao
author_sort Pok Man Hau
title Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle
title_short Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle
title_full Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle
title_fullStr Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle
title_full_unstemmed Epstein–Barr Virus Hijacks DNA Damage Response Transducers to Orchestrate Its Life Cycle
title_sort epstein–barr virus hijacks dna damage response transducers to orchestrate its life cycle
publisher MDPI AG
series Viruses
issn 1999-4915
publishDate 2017-11-01
description 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.
topic Epstein–Barr virus
DNA damage response
lytic reactivation
url https://www.mdpi.com/1999-4915/9/11/341
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AT saiwahtsao epsteinbarrvirushijacksdnadamageresponsetransducerstoorchestrateitslifecycle
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