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Biomolecules
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Immunity and Pathogenesis of Epstein-Barr Virus Infection
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Immunity and Pathogenesis of Epstein-Barr Virus Infection

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 10235

Special Issue Editor

Dr. Jonathan Kerr

E-Mail Website
Guest Editor
Department of Microbiology, Norfolk & Norwich University Hospitals NHS Foundation Trust, Norwich, UK
Interests: myalgic encephalomyelitis; chronic fatigue syndrome (ME/CFS); Epstein-Barr virus (EBV)
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Epstein–Barr virus (EBV) is a ubiquitous human virus which infects almost all humans during their lifetime and following the acute phase, persists for the remainder of the life of the individual. EBV infects B lymphocytes leading to their immortalisation, with persistence of the EBV genome as an episome. In the latent phase, EBV is prevented from reactivating through efficient cellular immunity. EBV reactivates (lytic phase) under conditions of psychological stress with consequent weakening of cellular immunity. EBV has been linked to development of many cancers and autoimmune diseases, through various mechanisms. This Special Issue will bring together topical aspects relating to EBV infection and its pathogenesis in autoimmune disease and cancer.

Dr. Jonathan Kerr
Guest Editor

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. Biomolecules 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
  • autoimmune disease
  • cancer
  • disease mechanism
  • pathogenesis

Published Papers (3 papers)

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Review

14 pages, 307 KiB  
Review
The Epstein-Barr Virus Hacks Immune Checkpoints: Evidence and Consequences for Lymphoproliferative Disorders and Cancers
by Alison Felipe Bordini Biggi and Deilson Elgui de Oliveira
Biomolecules 2022, 12(3), 397; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12030397 - 04 Mar 2022
Cited by 10 | Viewed by 2916
Abstract
The Epstein-Barr Virus (EBV) is a gammaherpesvirus involved in the etiopathogenesis of a variety of human cancers, mostly of lymphoid and epithelial origin. The EBV infection participates in both cell transformation and tumor progression, also playing an important role in subverting immune responses [...] Read more.
The Epstein-Barr Virus (EBV) is a gammaherpesvirus involved in the etiopathogenesis of a variety of human cancers, mostly of lymphoid and epithelial origin. The EBV infection participates in both cell transformation and tumor progression, also playing an important role in subverting immune responses against cancers. The homeostasis of the immune system is tightly regulated by inhibitory mechanisms affecting key immune effectors, such as T lymphocytes and NK cells. Collectively known as immune checkpoints, these mechanisms rely on a set of cellular receptors and ligands. These molecules may be candidate targets for immune checkpoints blockade—an emergent and promising modality of immunotherapy already proven to be valuable for a variety of human cancers. The EBV was lately suspected to interfere with the expression of immune checkpoint molecules, notably PD-1 and its ligands, found to be overexpressed in cases of Hodgkin lymphoma, nasopharyngeal, and gastric adenocarcinomas associated with the viral infection. Even though there is compelling evidence showing that the EBV interferes with other immune checkpoint regulators (e.g., CTLA-4, LAG-3, TIM-3, and VISTA), the published data are still scarce. Herein, we discuss the current state of the knowledge on how the EBV interferes with the activity of immune checkpoints regulators, as well as its implications considering the immune checkpoints blockade for clinical management of the EBV-associated malignancies, notably lymphomas. Full article
(This article belongs to the Special Issue Immunity and Pathogenesis of Epstein-Barr Virus Infection)
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Graphical abstract

12 pages, 901 KiB  
Review
Co-Stimulatory Molecules during Immune Control of Epstein Barr Virus Infection
by Christian Münz
Biomolecules 2022, 12(1), 38; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12010038 - 28 Dec 2021
Cited by 9 | Viewed by 2371
Abstract
The Epstein Barr virus (EBV) is one of the prominent human tumor viruses, and it is efficiently immune-controlled in most virus carriers. Cytotoxic lymphocytes strongly expand during symptomatic primary EBV infection and in preclinical in vivo models of this tumor virus infection. In [...] Read more.
The Epstein Barr virus (EBV) is one of the prominent human tumor viruses, and it is efficiently immune-controlled in most virus carriers. Cytotoxic lymphocytes strongly expand during symptomatic primary EBV infection and in preclinical in vivo models of this tumor virus infection. In these models and patients with primary immunodeficiencies, antibody blockade or deficiencies in certain molecular pathways lead to EBV-associated pathologies. In addition to T, NK, and NKT cell development, as well as their cytotoxic machinery, a set of co-stimulatory and co-inhibitory molecules was found to be required for EBV-specific immune control. The role of CD27/CD70, 4-1BB, SLAMs, NKG2D, CD16A/CD2, CTLA-4, and PD-1 will be discussed in this review. Some of these have just been recently identified as crucial for EBV-specific immune control, and for others, their important functions during protection were characterized in in vivo models of EBV infection and its immune control. These insights into the phenotype of cytotoxic lymphocytes that mediate the near-perfect immune control of EBV-associated malignancies might also guide immunotherapies against other tumors in the future. Full article
(This article belongs to the Special Issue Immunity and Pathogenesis of Epstein-Barr Virus Infection)
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Figure 1

15 pages, 784 KiB  
Review
Do Epstein–Barr Virus Mutations and Natural Genome Sequence Variations Contribute to Disease?
by Paul J. Farrell and Robert E. White
Biomolecules 2022, 12(1), 17; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12010017 - 23 Dec 2021
Cited by 17 | Viewed by 4167
Abstract
Most of the world’s population is infected by the Epstein–Barr virus (EBV), but the incidence of the diseases associated with EBV infection differs greatly in different parts of the world. Many factors may determine those differences, but variation in the virus genome is [...] Read more.
Most of the world’s population is infected by the Epstein–Barr virus (EBV), but the incidence of the diseases associated with EBV infection differs greatly in different parts of the world. Many factors may determine those differences, but variation in the virus genome is likely to be a contributing factor for some of the diseases. Here, we describe the main forms of EBV genome sequence variation, and the mechanisms by which variations in the virus genome are likely to contribute to disease. EBV genome deletions or polymorphisms can also provide useful markers for monitoring disease. If some EBV strains prove to be more pathogenic than others, this suggests the possible value of immunising people against infection by those pathogenic strains. Full article
(This article belongs to the Special Issue Immunity and Pathogenesis of Epstein-Barr Virus Infection)
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