Epstein Barr Virus

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

Deadline for manuscript submissions: closed (15 February 2021) | Viewed by 12817

Special Issue Editors


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Guest Editor
Laboratory of Lymphocyte Activation and Susceptibility to EBV, Inserrm UMR 1163, Imagine Institut, Université de Paris, Paris, France

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Guest Editor
Brigham & Women's Hospital, Harvard Medical School, 181 Longwood Avenue, Boston, MA 02115, USA
Interests: EBV; host-pathogen relationship; B-cell immunometabolism

Special Issue Information

Dear Colleagues,

The Epstein Barr virus (EBV) is an oncogenic virus of the gamma-herpes family with a marked tropism for epithelial cells and B lymphocytes, causing lymphoid and epithelial neoplasms. EBV contains more than 80 genes and 40 microRNAs. EBV is found all human populations, with more than 90% of individuals infected by the age of 25 years. Primary infection occurs in infancy and adolescence in most individuals, and is largely asymptomatic. In immune-competent individuals, EBV establishes a long-term persistent asymptomatic infection of B cells. In immunocompromised individuals, the persistence of EBV-infected cells is associated with severe pathologies, including hemophagocytic lymphohistiocytosis (HLH), as well as non-malignant and malignant lymphoproliferations. In this future monograph, leading scientists in the field of EBV will review the literature, highlight the recent progress that has been made through basic and clinical research, and provide their insights and views regarding various aspects of EBV biology, immune response to EBV, EBV-associated diseases and physiopathological mechanisms, EBV vaccination, etc.

Dr. Sylvain Latour
Dr. Benjamin Gewurz
Guest Editors

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Published Papers (4 papers)

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Review

27 pages, 1856 KiB  
Review
The Role of Coinfections in the EBV–Host Broken Equilibrium
by Yessica Sánchez-Ponce and Ezequiel M. Fuentes-Pananá
Viruses 2021, 13(7), 1399; https://0-doi-org.brum.beds.ac.uk/10.3390/v13071399 - 19 Jul 2021
Cited by 7 | Viewed by 4637
Abstract
The Epstein–Barr virus (EBV) is a well-adapted human virus, and its infection is exclusive to our species, generally beginning in the childhood and then persisting throughout the life of most of the affected adults. Although this infection generally remains asymptomatic, EBV can trigger [...] Read more.
The Epstein–Barr virus (EBV) is a well-adapted human virus, and its infection is exclusive to our species, generally beginning in the childhood and then persisting throughout the life of most of the affected adults. Although this infection generally remains asymptomatic, EBV can trigger life-threatening conditions under unclear circumstances. The EBV lifecycle is characterized by interactions with other viruses or bacteria, which increases the probability of awakening its pathobiont capacity. For instance, EBV infects B cells with the potential to alter the germinal center reaction (GCR)—an adaptive immune structure wherein mutagenic-driven processes take place. HIV- and Plasmodium falciparum-induced B cell hyperactivation also feeds the GCR. These agents, along with the B cell tropic KSHV, converge in the ontogeny of germinal center (GC) or post-GC lymphomas. EBV oral transmission facilitates interactions with local bacteria and HPV, thereby increasing the risk of periodontal diseases and head and neck carcinomas. It is less clear as to how EBV is localized in the stomach, but together with Helicobacter pylori, they are known to be responsible for gastric cancer. Perhaps this mechanism is reminiscent of the local inflammation that attracts different herpesviruses and enhances graft damage and chances of rejection in transplanted patients. In this review, we discussed the existing evidence suggestive of EBV possessing the potential to synergize or cooperate with these agents to trigger or worsen the disease. Full article
(This article belongs to the Special Issue Epstein Barr Virus)
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15 pages, 831 KiB  
Review
Pathogenic Role of Epstein–Barr Virus in Lung Cancers
by David Becnel, Ramsy Abdelghani, Asuka Nanbo, Janardhan Avilala, Jacob Kahn, Li Li and Zhen Lin
Viruses 2021, 13(5), 877; https://0-doi-org.brum.beds.ac.uk/10.3390/v13050877 - 11 May 2021
Cited by 14 | Viewed by 2898
Abstract
Human oncogenic viruses account for at least 12% of total cancer cases worldwide. Epstein–Barr virus (EBV) is the first identified human oncogenic virus and it alone causes ~200,000 cancer cases and ~1.8% of total cancer-related death annually. Over the past 40 years, increasing [...] Read more.
Human oncogenic viruses account for at least 12% of total cancer cases worldwide. Epstein–Barr virus (EBV) is the first identified human oncogenic virus and it alone causes ~200,000 cancer cases and ~1.8% of total cancer-related death annually. Over the past 40 years, increasing lines of evidence have supported a causal link between EBV infection and a subgroup of lung cancers (LCs). In this article, we review the current understanding of the EBV-LC association and the etiological role of EBV in lung carcinogenesis. We also discuss the clinical impact of the knowledge gained from previous research, challenges, and future directions in this field. Given the high clinical relevance of EBV-LC association, there is an urgent need for further investigation on this topic. Full article
(This article belongs to the Special Issue Epstein Barr Virus)
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11 pages, 1295 KiB  
Review
Inflammasome, the Constitutive Heterochromatin Machinery, and Replication of an Oncogenic Herpesvirus
by Sumita Bhaduri-McIntosh and Michael T. McIntosh
Viruses 2021, 13(5), 846; https://0-doi-org.brum.beds.ac.uk/10.3390/v13050846 - 06 May 2021
Cited by 7 | Viewed by 2526
Abstract
The success of long-term host–virus partnerships is predicated on the ability of the host to limit the destructive potential of the virus and the virus’s skill in manipulating its host to persist undetected yet replicate efficiently when needed. By mastering such skills, herpesviruses [...] Read more.
The success of long-term host–virus partnerships is predicated on the ability of the host to limit the destructive potential of the virus and the virus’s skill in manipulating its host to persist undetected yet replicate efficiently when needed. By mastering such skills, herpesviruses persist silently in their hosts, though perturbations in this host–virus equilibrium can result in disease. The heterochromatin machinery that tightly regulates endogenous retroviral elements and pericentromeric repeats also silences invading genomes of alpha-, beta-, and gammaherpesviruses. That said, how these viruses disrupt this constitutive heterochromatin machinery to replicate and spread, particularly in response to disparate lytic triggers, is unclear. Here, we review how the cancer-causing gammaherpesvirus Epstein–Barr virus (EBV) uses the inflammasome as a security system to alert itself of threats to its cellular home as well as to flip the virus-encoded lytic switch, allowing it to replicate and escape in response to a variety of lytic triggers. EBV provides the first example of an infectious agent able to actively exploit the inflammasome to spark its replication. Revealing an unexpected link between the inflammasome and the epigenome, this further brings insights into how the heterochromatin machinery uses differential strategies to maintain the integrity of the cellular genome whilst guarding against invading pathogens. These recent insights into EBV biology and host–viral epigenetic regulation ultimately point to the NLRP3 inflammasome as an attractive target to thwart herpesvirus reactivation. Full article
(This article belongs to the Special Issue Epstein Barr Virus)
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8 pages, 903 KiB  
Review
Epstein–Barr Virus and Peri-Implantitis: A Systematic Review and Meta-Analysis
by Elisabet Roca-Millan, Judith Domínguez-Mínger, Mayra Schemel-Suárez, Albert Estrugo-Devesa, Antonio Marí-Roig and José López-López
Viruses 2021, 13(2), 250; https://0-doi-org.brum.beds.ac.uk/10.3390/v13020250 - 05 Feb 2021
Cited by 2 | Viewed by 1850
Abstract
The exponential growth in the use of dental implants in the last decades has been accompanied by an increase in the prevalence of peri-implant disease. It appears that viruses may have pathogenic potential for the development of this pathology. The objective of this [...] Read more.
The exponential growth in the use of dental implants in the last decades has been accompanied by an increase in the prevalence of peri-implant disease. It appears that viruses may have pathogenic potential for the development of this pathology. The objective of this systematic review is to study the possible association between the presence of Epstein–Barr virus and the development of peri-implantitis. An electronic search was conducted in PubMed/MEDLINE, Scielo and Embase databases for cross-sectional and case–control studies in humans published up to and including 4 January 2021. Five studies were included in the qualitative analysis. The meta-analysis did not show a statistically significant difference regarding the prevalence of Epstein–Barr virus in the peri-implant sulcus between implants with peri-implantitis and healthy implants. In conclusion, no association between the human herpesvirus 4 and peri-implantitis was found. Further research on this topic is essential to develop more effective treatments. Full article
(This article belongs to the Special Issue Epstein Barr Virus)
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