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Pathogens
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Emerging Topics in Epstein-Barr virus-Associated Diseases
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Emerging Topics in Epstein-Barr virus-Associated Diseases

A special issue of Pathogens (ISSN 2076-0817).

Deadline for manuscript submissions: closed (31 May 2018) | Viewed by 40815

Special Issue Editors

Prof. Dr. Paul Murray

E-Mail Website
Guest Editor
Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham B15 2TT, UK
Interests: lymphoma; diffuse large B cell lymphoma; Hodgkin lymphoma; Epstein–Barr virus; nasopharyngeal carcinoma
Special Issues, Collections and Topics in MDPI journals
Dr. Graham Taylor

E-Mail
Guest Editor
University of Birmingham
Interests: Epstein-Barr virus; nasopharyngeal carcinoma; B cell lymphoma; therapeutic vaccination
Dr. Lee-Fah Yap

E-Mail
Guest Editor
Universiti of Malaya
Interests: Epstein-Barr virus; nasopharyngeal carcinoma; cell signalling

Special Issue Information

Dear Colleagues,

Although the association between EBV and a variety of human diseases is well documented, how the virus contributes to the pathogenesis of these different diseases remains only poorly understood. This Special Issue seeks to synthesise new knowledge of EBV’s contribution to the pathogenesis of the wide range of associated diseases, focusing, not just on cancer, but also on other associations; for example, autoimmune disorders. In doing so, it will bring together emerging new themes in EBV biology, while at the same time attempting to define the important outstanding research questions in the field. It will also highlight how our developing knowledge of how virus–host interactions are perturbed in disease could help to inform the development of novel therapeutics and diagnostics for patients with EBV-associated disorders.

Prof. Paul Murray
Dr. Lee-Fah Yap
Dr. Graham Taylor
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Pathogens is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Epstein-Barr virus
  • cancer
  • autoimmunity
  • epidemiology

Published Papers (5 papers)

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Review

11 pages, 420 KiB  
Review
Epstein-Barr Virus-Induced Epigenetic Pathogenesis of Viral-Associated Lymphoepithelioma-Like Carcinomas and Natural Killer/T-Cell Lymphomas
by Lili Li, Brigette B. Y. Ma, Anthony T. C. Chan, Francis K. L. Chan, Paul Murray and Qian Tao
Pathogens 2018, 7(3), 63; https://doi.org/10.3390/pathogens7030063 - 18 Jul 2018
Cited by 18 | Viewed by 8769
Abstract
Cancer genome studies of Epstein-Barr virus (EBV)-associated tumors, including lymphoepithelioma-like carcinomas (LELC) of nasopharyngeal (NPC), gastric (EBVaGC) and lung tissues, and natural killer (NK)/T-cell lymphoma (NKTCL), reveal a unique feature of genomic alterations with fewer gene mutations detected than other common cancers. It [...] Read more.
Cancer genome studies of Epstein-Barr virus (EBV)-associated tumors, including lymphoepithelioma-like carcinomas (LELC) of nasopharyngeal (NPC), gastric (EBVaGC) and lung tissues, and natural killer (NK)/T-cell lymphoma (NKTCL), reveal a unique feature of genomic alterations with fewer gene mutations detected than other common cancers. It is known now that epigenetic alterations play a critical role in the pathogenesis of EBV-associated tumors. As an oncogenic virus, EBV establishes its latent and lytic infections in B-lymphoid and epithelial cells, utilizing hijacked cellular epigenetic machinery. EBV-encoded oncoproteins modulate cellular epigenetic machinery to reprogram viral and host epigenomes, especially in the early stage of infection, using host epigenetic regulators. The genome-wide epigenetic alterations further inactivate a series of tumor suppressor genes (TSG) and disrupt key cellular signaling pathways, contributing to EBV-associated cancer initiation and progression. Profiling of genome-wide CpG methylation changes (CpG methylome) have revealed a unique epigenotype of global high-grade methylation of TSGs in EBV-associated tumors. Here, we have summarized recent advances of epigenetic alterations in EBV-associated tumors (LELCs and NKTCL), highlighting the importance of epigenetic etiology in EBV-associated tumorigenesis. Epigenetic study of these EBV-associated tumors will discover valuable biomarkers for their early detection and prognosis prediction, and also develop effective epigenetic therapeutics for these cancers. Full article
(This article belongs to the Special Issue Emerging Topics in Epstein-Barr virus-Associated Diseases)
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17 pages, 680 KiB  
Review
Contribution of Epstein–Barr Virus Latent Proteins to the Pathogenesis of Classical Hodgkin Lymphoma
by Katerina Vrzalikova, Taofik Sunmonu, Gary Reynolds and Paul Murray
Pathogens 2018, 7(3), 59; https://doi.org/10.3390/pathogens7030059 - 27 Jun 2018
Cited by 19 | Viewed by 4908
Abstract
Pathogenic viruses have evolved to manipulate the host cell utilising a variety of strategies including expression of viral proteins to hijack or mimic the activity of cellular functions. DNA tumour viruses often establish latent infection in which no new virions are produced, characterized [...] Read more.
Pathogenic viruses have evolved to manipulate the host cell utilising a variety of strategies including expression of viral proteins to hijack or mimic the activity of cellular functions. DNA tumour viruses often establish latent infection in which no new virions are produced, characterized by the expression of a restricted repertoire of so-called latent viral genes. These latent genes serve to remodel cellular functions to ensure survival of the virus within host cells, often for the lifetime of the infected individual. However, under certain circumstances, virus infection may contribute to transformation of the host cell; this event is not a usual outcome of infection. Here, we review how the Epstein–Barr virus (EBV), the prototypic oncogenic human virus, modulates host cell functions, with a focus on the role of the EBV latent genes in classical Hodgkin lymphoma. Full article
(This article belongs to the Special Issue Emerging Topics in Epstein-Barr virus-Associated Diseases)
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23 pages, 4273 KiB  
Review
The Microenvironment in Epstein–Barr Virus-Associated Malignancies
by Geok Wee Tan, Lydia Visser, Lu Ping Tan, Anke Van den Berg and Arjan Diepstra
Pathogens 2018, 7(2), 40; https://doi.org/10.3390/pathogens7020040 - 13 Apr 2018
Cited by 39 | Viewed by 7795
Abstract
The Epstein–Barr virus (EBV) can cause a wide variety of cancers upon infection of different cell types and induces a highly variable composition of the tumor microenvironment (TME). This TME consists of both innate and adaptive immune cells and is not merely an [...] Read more.
The Epstein–Barr virus (EBV) can cause a wide variety of cancers upon infection of different cell types and induces a highly variable composition of the tumor microenvironment (TME). This TME consists of both innate and adaptive immune cells and is not merely an aspecific reaction to the tumor cells. In fact, latent EBV-infected tumor cells utilize several specific mechanisms to form and shape the TME to their own benefit. These mechanisms have been studied largely in the context of EBV+ Hodgkin lymphoma, undifferentiated nasopharyngeal carcinoma, and EBV+ gastric cancer. This review describes the composition, immune escape mechanisms, and tumor cell promoting properties of the TME in these three malignancies. Mechanisms of susceptibility which regularly involve genes related to immune system function are also discussed, as only a small proportion of EBV-infected individuals develops an EBV-associated malignancy. Full article
(This article belongs to the Special Issue Emerging Topics in Epstein-Barr virus-Associated Diseases)
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15 pages, 2333 KiB  
Review
The Cooperative Functions of the EBNA3 Proteins Are Central to EBV Persistence and Latency
by Christine T. Styles, Kostas Paschos, Robert E. White and Paul J. Farrell
Pathogens 2018, 7(1), 31; https://doi.org/10.3390/pathogens7010031 - 17 Mar 2018
Cited by 26 | Viewed by 6195
Abstract
The Epstein–Barr nuclear antigen 3 (EBNA3) family of proteins, comprising EBNA3A, EBNA3B, and EBNA3C, play pivotal roles in the asymptomatic persistence and life-long latency of Epstein–Barr virus (EBV) in the worldwide human population. EBNA3-mediated transcriptional reprogramming of numerous host cell genes promotes in [...] Read more.
The Epstein–Barr nuclear antigen 3 (EBNA3) family of proteins, comprising EBNA3A, EBNA3B, and EBNA3C, play pivotal roles in the asymptomatic persistence and life-long latency of Epstein–Barr virus (EBV) in the worldwide human population. EBNA3-mediated transcriptional reprogramming of numerous host cell genes promotes in vitro B cell transformation and EBV persistence in vivo. Despite structural and sequence similarities, and evidence of substantial cooperative activity between the EBNA3 proteins, they perform quite different, often opposing functions. Both EBNA3A and EBNA3C are involved in the repression of important tumour suppressive pathways and are considered oncogenic. In contrast, EBNA3B exhibits tumour suppressive functions. This review focuses on how the EBNA3 proteins achieve the delicate balance required to support EBV persistence and latency, with emphasis on the contribution of the Allday laboratory to the field of EBNA3 biology. Full article
(This article belongs to the Special Issue Emerging Topics in Epstein-Barr virus-Associated Diseases)
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45 pages, 13782 KiB  
Review
EBV-Positive Lymphoproliferations of B- T- and NK-Cell Derivation in Non-Immunocompromised Hosts
by Stefan D. Dojcinov, Falko Fend and Leticia Quintanilla-Martinez
Pathogens 2018, 7(1), 28; https://doi.org/10.3390/pathogens7010028 - 07 Mar 2018
Cited by 87 | Viewed by 12297
Abstract
The contribution of Epstein-Barr virus (EBV) to the development of specific types of benign lymphoproliferations and malignant lymphomas has been extensively studied since the discovery of the virus over the last 50 years. The importance and better understanding of the EBV-associated lymphoproliferative disorders [...] Read more.
The contribution of Epstein-Barr virus (EBV) to the development of specific types of benign lymphoproliferations and malignant lymphomas has been extensively studied since the discovery of the virus over the last 50 years. The importance and better understanding of the EBV-associated lymphoproliferative disorders (LPD) of B, T or natural killer (NK) cell type has resulted in the recognition of new entities like EBV+ mucocutaneous ulcer or the addition of chronic active EBV (CAEBV) infection in the revised 2016 World Health Organization (WHO) lymphoma classification. In this article, we review the definitions, morphology, pathogenesis, and evolving concepts of the various EBV-associated disorders including EBV+ diffuse large B-cell lymphoma, not otherwise specified (DLBCL, NOS), EBV+ mucocutaneous ulcer, DLBCL associated with chronic inflammation, fibrin-associated DLBCL, lymphomatoid granulomatosis, the EBV+ T and NK-cell LPD of childhood, aggressive NK leukaemia, extranodal NK/T-cell lymphoma, nasal type, and the new provisional entity of primary EBV+ nodal T- or NK-cell lymphoma. The current knowledge regarding the pathogenesis of B-cell lymphomas that can be EBV-associated including Burkitt lymphoma, plasmablastic lymphoma and classic Hodgkin lymphoma will be also explored. Full article
(This article belongs to the Special Issue Emerging Topics in Epstein-Barr virus-Associated Diseases)
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