Epstein–Barr virus and autoimmunity: the role of a latent viral infection in multiple sclerosis and systemic lupus erythematosus pathogenesis

2013 ◽  
Vol 8 (2) ◽  
pp. 173-182 ◽  
Author(s):  
Costanza Casiraghi ◽  
Marc S Horwitz
Keyword(s):  
Multiple Sclerosis ◽  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Systemic Lupus ◽  
Barr Virus ◽  
Systemic Lupus Erythematosus Pathogenesis ◽  
Latent Viral Infection ◽  
Epstein Barr

scholarly journals Epstein Barr Virus and Autoimmune Responses in Systemic Lupus Erythematosus

2021 ◽  
Vol 11 ◽  
Author(s):  
Neelakshi R. Jog ◽  
Judith A. James
Keyword(s):  
Multiple Sclerosis ◽  
Systemic Lupus Erythematosus ◽  
Systemic Sclerosis ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Immune Dysregulation ◽  
Systemic Autoimmune Disease ◽  
Systemic Lupus ◽  
Barr Virus ◽  
Epstein Barr

Systemic lupus erythematosus (SLE) is a complex systemic autoimmune disease. Infections or infectious reactivation are potential triggers for initiation of autoimmunity and for SLE flares. Epstein-Barr virus (EBV) is gamma herpes virus that has been associated with several autoimmune diseases such as SLE, multiple sclerosis, Sjogren’s syndrome, and systemic sclerosis. In this review, we will discuss the recent advances regarding how EBV may contribute to immune dysregulation, and how these mechanisms may relate to SLE disease progression.

scholarly journals Epstein-Barr Virus in Systemic Lupus Erythematosus, Rheumatoid Arthritis and Multiple Sclerosis—Association and Causation

Viruses ◽  
2012 ◽  
Vol 4 (12) ◽  
pp. 3701-3730 ◽  
Author(s):  
Andreas Lossius ◽  
Jorunn Johansen ◽  
Øivind Torkildsen ◽  
Frode Vartdal ◽  
Trygve Holmøy
Keyword(s):  
Rheumatoid Arthritis ◽  
Multiple Sclerosis ◽  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Systemic Lupus ◽  
Barr Virus ◽  
Epstein Barr

scholarly journals Viral Infections and Systemic Lupus Erythematosus: New Players in an Old Story

Viruses ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 277 ◽  
Author(s):  
Marco Quaglia ◽  
Guido Merlotti ◽  
Marco De Andrea ◽  
Cinzia Borgogna ◽  
Vincenzo Cantaluppi
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune Response ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Viral Infections ◽  
Systemic Lupus ◽  
Barr Virus ◽  
Epstein Barr ◽  
The Impact

A causal link between viral infections and autoimmunity has been studied for a long time and the role of some viruses in the induction or exacerbation of systemic lupus erythematosus (SLE) in genetically predisposed patients has been proved. The strength of the association between different viral agents and SLE is variable. Epstein–Barr virus (EBV), parvovirus B19 (B19V), and human endogenous retroviruses (HERVs) are involved in SLE pathogenesis, whereas other viruses such as Cytomegalovirus (CMV) probably play a less prominent role. However, the mechanisms of viral–host interactions and the impact of viruses on disease course have yet to be elucidated. In addition to classical mechanisms of viral-triggered autoimmunity, such as molecular mimicry and epitope spreading, there has been a growing appreciation of the role of direct activation of innate response by viral nucleic acids and epigenetic modulation of interferon-related immune response. The latter is especially important for HERVs, which may represent the molecular link between environmental triggers and critical immune genes. Virus-specific proteins modulating interaction with the host immune system have been characterized especially for Epstein–Barr virus and explain immune evasion, persistent infection and self-reactive B-cell “immortalization”. Knowledge has also been expanding on key viral proteins of B19-V and CMV and their possible association with specific phenotypes such as antiphospholipid syndrome. This progress may pave the way to new therapeutic perspectives, including the use of known or new antiviral drugs, postviral immune response modulation and innate immunity inhibition. We herein describe the state-of-the-art knowledge on the role of viral infections in SLE, with a focus on their mechanisms of action and potential therapeutic targets.

scholarly journals Epstein–Barr Virus in Salivary Samples from Systemic Lupus Erythematosus Patients with Oral Lesions

2021 ◽  
Vol 10 (21) ◽  
pp. 4995
Author(s):  
Alessio Buonavoglia ◽  
Patrizia Leone ◽  
Marcella Prete ◽  
Antonio Giovanni Solimando ◽  
Chiara Guastadisegno ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Epstein Barr Virus ◽  
Oral Lesions ◽  
Systemic Lupus ◽  
Real Time Quantitative Pcr ◽  
Barr Virus ◽  
Ebv Dna ◽  
Epstein Barr

In order to investigate the possible role of Epstein–Barr virus (EBV) in systemic lupus erythematosus (SLE) and its associated oral lesions, a pilot case–control study was performed. A total of 31 patients (18 females and 13 males) were enrolled in the study and divided into two groups: group A included 16 patients with diagnosis of SLE and group B included 15 healthy individuals. Salivary swab samples were collected and subjected to molecular screening by real-time quantitative PCR (qPCR) for the detection of EBV DNA. EBV DNA was significantly detected in 8/16 (50%) SLE patients and in 5/7 (71.4%) subjects with SLE-associated oral lesions. Since EBV is one of the most common viruses in the human population, it is difficult to understand if it is the causative agent of SLE or, vice versa, if SLE is able to trigger the reactivation of EBV. This study highlights a significant association between the presence of EBV and both SLE and SLE-related oral lesions and provides rationale for further investigation into the role of EBV in SLE pathogenesis.

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