Special Issue "EBV and Autoimmune Disease"

A special issue of Microorganisms (ISSN 2076-2607). This special issue belongs to the section "Medical Microbiology".

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 2269

Special Issue Editor

Dr. Antonella Farina
E-Mail Website
Guest Editor
Institute Pasteur-Fondazione Cenci Bolognetti, Department of Experimental Medicine, "Sapienza", University of Rome, Rome, Italy
Interests: virus infection

Special Issue Information

Dear Colleagues,

Epstein–Barr Virus (EBV), the first human tumor virus, was identified more than 50 years ago.

Primary infection generally occurs in the oropharynx; EBV then crosses the basal membrane of oral epithelium to reach B lymphocytes, into which it establishes a lifelong latent infection. EBV reactivation from latency induces host cells to differentiate into plasma cells as the virus starts expressing proteins of the lytic cycle to produce infectious progeny.

Whilst much of what is known about EBV comes from its association with cancer, emerging evidence suggests that the virus may also play a critical role in pathogenesis of several autoimmune diseases, thus adding another complexity to the mosaic of autoimmunity. The large diffusion of this virus (95% people worldwide are infected) and the fact that EBV lodges in B lymphocytes, fundamental for adaptive humoral immunity, suggest a delicate balance between the virus and immune responses. Decades of research into how EBV escapes immune eradication has provided important information regarding the virus–host interaction, but the new challenge today is to clarify how EBV controls and triggers immune response and, as a consequence, sometimes leads to aberrant autoimmune reactions.

The aim of this Special Issue is to provide insights into the interaction between EBV and autoimmune diseases. To this end, I would like to invite you to submit your research/review articles, and short communications related to EBV and Autoimmunity.

As a Guest Editor of this Special Issue, I look forward to reviewing your submissions and, together, defining the present state of the art as to how this common herpesvirus contributes to debilitating autoimmune diseases.

Dr. Antonella Farina
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.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 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 and immune response
  • systemic sclerosis, multiple sclerosis
  • systemic autoimmune diseases
  • SLE
  • RA

Published Papers (1 paper)

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Review

Review
Epstein Barr Virus Exploits Genetic Susceptibility to Increase Multiple Sclerosis Risk
Microorganisms 2021, 9(11), 2191; https://doi.org/10.3390/microorganisms9112191 - 21 Oct 2021
Cited by 2 | Viewed by 1822
Abstract
Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) for which both genetic and environmental risk factors have been identified. The strongest synergy among them exists between the MHC class II haplotype and infection with the Epstein Barr virus [...] Read more.
Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) for which both genetic and environmental risk factors have been identified. The strongest synergy among them exists between the MHC class II haplotype and infection with the Epstein Barr virus (EBV), especially symptomatic primary EBV infection (infectious mononucleosis) and elevated EBV-specific antibodies. In this review, we will summarize the epidemiological evidence that EBV infection is a prerequisite for MS development, describe altered EBV specific immune responses in MS patients, and speculate about possible pathogenic mechanisms for the synergy between EBV infection and the MS-associated MHC class II haplotype. We will also discuss how at least one of these mechanisms might explain the recent success of B cell-depleting therapies for MS. While a better mechanistic understanding of the role of EBV infection and its immune control during MS pathogenesis is required and calls for the development of innovative experimental systems to test the proposed mechanisms, therapies targeting EBV-infected B cells are already starting to be explored in MS patients. Full article
(This article belongs to the Special Issue EBV and Autoimmune Disease)
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