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Special Issue "Recent Progress in EBV Research"

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A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (31 December 2013)

Special Issue Editor

Guest Editor
Prof. Dr. Eric C. Johannsen

Assistant Professor, Morgridge Institute for Research, University of Wisconsin, 330 N. Orchard St., Room 3268, Madison, WI 53717, USA
Website | E-Mail

Special Issue Information

Submission

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. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as 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 refereed through a peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses 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 1500 CHF (Swiss Francs).

Keywords

  • Epstein-Barr Virus
  • EBV
  • viral oncogenesis
  • herpesvirus
  • gammaherpesvirus
  • viral latency
  • growth transformation
  • replication
  • lymphoma
  • burkitt lymphoma
  • hodgkin lymphoma
  • lymphoproliferative disease nasopharyngeal carcinoma
  • gastric carcinoma
  • infectious mononucleosis

Published Papers (6 papers)

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Research

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Open AccessArticle Evidence of Epstein-Barr Virus Association with Gastric Cancer and Non-Atrophic Gastritis
Viruses 2014, 6(1), 301-318; doi:10.3390/v6010301
Received: 26 August 2013 / Revised: 8 December 2013 / Accepted: 6 January 2014 / Published: 20 January 2014
Cited by 9 | PDF Full-text (1559 KB) | HTML Full-text | XML Full-text
Abstract
Different lines of evidence support an association between Epstein-Barr virus (EBV) and gastric cancer (GC). The main understood risk factor to develop GC is infection by Helicobacter pylori (H. pylori), which triggers a local inflammatory response critical for progression from gastritis
[...] Read more.
Different lines of evidence support an association between Epstein-Barr virus (EBV) and gastric cancer (GC). The main understood risk factor to develop GC is infection by Helicobacter pylori (H. pylori), which triggers a local inflammatory response critical for progression from gastritis to GC. The role of EBV in early inflammatory gastric lesions has been poorly studied. A recent study proposed a cutoff value of 2000 EBV particles to identify patients with increased chances of infection of the gastric epithelium, which may favor the inflammatory process. To better understand the role of EBV in cancer progression, we analyzed 75 samples of GC, 147 control samples of non-tumor gastric tissue derived from GC patients and 75 biopsies from patients with non-atrophic gastritis (NAG). A first-round PCR was used for EBV detection in tumor and non-tumor controls and a more sensitive nested PCR for gastritis samples; both PCRs had lower detection limits above the proposed cutoff value. With this strategy 10.67% of GC, 1.3% of non-tumor controls and 8% of gastritis samples were found positive. An EBER1 in situ hybridization showed EBV infection of epithelial cells in GC and in a third of NAG samples, while in the other NAGs infection was restricted to the mononuclear cell infiltrate. EBV-positive GCs were enriched in lace and cribriform patterns, while these rare patterns were not observed in EBV negative samples. Our results support a role for EBV in GC and early precursor lesions, either as directly oncogenic infecting epithelial cells or indirectly as an inflammatory trigger. Full article
(This article belongs to the Special Issue Recent Progress in EBV Research)

Review

Jump to: Research, Other

Open AccessReview NF-κB and IRF7 Pathway Activation by Epstein-Barr Virus Latent Membrane Protein 1
Viruses 2013, 5(6), 1587-1606; doi:10.3390/v5061587
Received: 28 May 2013 / Revised: 17 June 2013 / Accepted: 18 June 2013 / Published: 21 June 2013
Cited by 17 | PDF Full-text (6837 KB) | HTML Full-text | XML Full-text
Abstract
The principal Epstein-Barr virus (EBV) oncoprotein, Latent Membrane Protein 1 (LMP1), is expressed in most EBV-associated human malignancies. LMP1 mimics CD40 receptor signaling to provide infected cells with constitutive NF-κB, MAP kinase, IRF7, and PI3 kinase pathway stimulation. EBV-transformed B-cells are particularly dependent
[...] Read more.
The principal Epstein-Barr virus (EBV) oncoprotein, Latent Membrane Protein 1 (LMP1), is expressed in most EBV-associated human malignancies. LMP1 mimics CD40 receptor signaling to provide infected cells with constitutive NF-κB, MAP kinase, IRF7, and PI3 kinase pathway stimulation. EBV-transformed B-cells are particularly dependent on constitutive NF-κB activity, and rapidly undergo apoptosis upon NF-κB blockade. Here, we review LMP1 function, with special attention to current understanding of the molecular mechanisms of LMP1-mediated NF-κB and IRF7 pathway activation. Recent advances include the elucidation of transmembrane motifs important for LMP1 trafficking and ligand-independent signaling, analysis of genome-wide LMP1 gene targets, and the identification of novel cell proteins that mediate LMP1 NF-κB and IRF7 pathway activation. Full article
(This article belongs to the Special Issue Recent Progress in EBV Research)
Open AccessReview Potential Cellular Functions of Epstein-Barr Nuclear Antigen 1 (EBNA1) of Epstein-Barr Virus
Viruses 2013, 5(1), 226-240; doi:10.3390/v5010226
Received: 5 December 2012 / Revised: 23 December 2012 / Accepted: 11 January 2013 / Published: 16 January 2013
Cited by 20 | PDF Full-text (260 KB) | HTML Full-text | XML Full-text
Abstract
Epstein-Barr Nuclear Antigen 1 (EBNA1) is a multifunctional protein encoded by EBV. EBNA1’s role in maintaining EBV in latently proliferating cells, by mediating EBV genome synthesis and nonrandom partitioning to daughter cells, as well as regulating viral gene transcription, is well characterized. Less
[...] Read more.
Epstein-Barr Nuclear Antigen 1 (EBNA1) is a multifunctional protein encoded by EBV. EBNA1’s role in maintaining EBV in latently proliferating cells, by mediating EBV genome synthesis and nonrandom partitioning to daughter cells, as well as regulating viral gene transcription, is well characterized. Less understood are the roles of EBNA1 in affecting the host cell to provide selective advantages to those cells that harbor EBV. In this review we will focus on the interactions between EBNA1 and the host cell that may provide EBV-infected cells selective advantages beyond the maintenance of EBV. Full article
(This article belongs to the Special Issue Recent Progress in EBV Research)
Open AccessReview Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation
Viruses 2012, 4(12), 3701-3730; doi:10.3390/v4123701
Received: 31 October 2012 / Revised: 6 December 2012 / Accepted: 7 December 2012 / Published: 13 December 2012
Cited by 35 | PDF Full-text (489 KB) | HTML Full-text | XML Full-text
Abstract
Epidemiological data suggest that the Epstein-Barr virus (EBV) is associated with several autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis. However, it is not clear whether EBV plays a role in the pathogenesis of these diseases, and if so,
[...] Read more.
Epidemiological data suggest that the Epstein-Barr virus (EBV) is associated with several autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis and multiple sclerosis. However, it is not clear whether EBV plays a role in the pathogenesis of these diseases, and if so, by which mechanisms the virus may contribute. In this review, we discuss possible viral and immunological mechanisms that might explain associations between EBV and autoimmune diseases and whether these associations represent causes or effects of inflammation and autoimmunity. Full article
(This article belongs to the Special Issue Recent Progress in EBV Research)
Open AccessReview Epstein-Barr Virus (EBV)-associated Gastric Carcinoma
Viruses 2012, 4(12), 3420-3439; doi:10.3390/v4123420
Received: 22 October 2012 / Revised: 22 November 2012 / Accepted: 26 November 2012 / Published: 29 November 2012
Cited by 55 | PDF Full-text (1191 KB) | HTML Full-text | XML Full-text
Abstract
The ubiquitous Epstein-Barr virus (EBV) is associated with several human tumors, which include lymphoid and epithelial malignancies. It is known that EBV persistently infects the memory B cell pool of healthy individuals by activating growth and survival signaling pathways that can contribute to
[...] Read more.
The ubiquitous Epstein-Barr virus (EBV) is associated with several human tumors, which include lymphoid and epithelial malignancies. It is known that EBV persistently infects the memory B cell pool of healthy individuals by activating growth and survival signaling pathways that can contribute to B cell lymphomagenesis.  Although the monoclonal proliferation of EBV-infected cells can be observed in epithelial tumors, such as nasopharyngeal carcinoma and EBV-associated gastric carcinoma, the precise role of EBV in the carcinogenic progress is not fully understood. This review features characteristics and current understanding of EBV-associated gastric carcinoma. EBV-associated gastric carcinoma comprises almost 10% of all gastric carcinoma cases and expresses restricted EBV latent genes (Latency I). Firstly, definition, epidemiology, and clinical features are discussed. Then, the route of infection and carcinogenic role of viral genes are presented.  Of particular interest, the association with frequent genomic CpG methylation and role of miRNA for carcinogenesis are topically discussed. Finally, the possibility of therapies targeting EBV-associated gastric carcinoma is proposed. Full article
(This article belongs to the Special Issue Recent Progress in EBV Research)

Other

Jump to: Research, Review

Open AccessCommentary Interpreting the Epstein-Barr Virus (EBV) Epigenome Using High-Throughput Data
Viruses 2013, 5(4), 1042-1054; doi:10.3390/v5041042
Received: 18 February 2013 / Revised: 11 March 2013 / Accepted: 18 March 2013 / Published: 2 April 2013
Cited by 16 | PDF Full-text (1142 KB) | HTML Full-text | XML Full-text
Abstract
The Epstein-Barr virus (EBV) double-stranded DNA genome is subject to extensive epigenetic regulation. Large consortiums and individual labs have generated a vast number of genome-wide data sets on human lymphoblastoid and other cell lines latently infected with EBV. Analysis of these data sets
[...] Read more.
The Epstein-Barr virus (EBV) double-stranded DNA genome is subject to extensive epigenetic regulation. Large consortiums and individual labs have generated a vast number of genome-wide data sets on human lymphoblastoid and other cell lines latently infected with EBV. Analysis of these data sets reveals important new information on the properties of the host and viral chromosome structure organization and epigenetic modifications. We discuss the mapping of these data sets and the subsequent insights into the chromatin structure and transcription factor binding patterns on latent EBV genomes. Colocalization of multiple histone modifications and transcription factors at regulatory loci are considered in the context of the biology and regulation of EBV. Full article
(This article belongs to the Special Issue Recent Progress in EBV Research)

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