Epstein-Barr Virus in Systemic Autoimmune Diseases

Abstract

Systemic autoimmune diseases (SADs) are a group of connective tissue diseases with diverse, yet overlapping, symptoms and autoantibody development. The etiology behind SADs is not fully elucidated, but a number of genetic and environmental factors are known to influence the incidence of SADs. Recent findings link dysregulation of Epstein-Barr virus (EBV) with SAD development. EBV causes a persistent infection with a tight latency programme in memory B-cells, which enables evasion of the immune defence. A number of immune escape mechanisms and immune-modulating proteins have been described for EBV. These immune modulating functions make EBV a good candidate for initiation of autoimmune diseases and exacerbation of disease progression. This review focuses on systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and Sjögren's syndrome (SS) and sum up the existing data linking EBV with these diseases including elevated titres of EBV antibodies, reduced T-cell defence against EBV, and elevated EBV viral load. Together, these data suggest that uncontrolled EBV infection can develop diverse autoreactivities in genetic susceptible individuals with different manifestations depending on the genetic background and the site of reactivation.

Burkitt’s Lymphoma in a patient with systemic lupus erythematosus

“…Increased viral load, EBV mRNA expression, and EBV-directed antibodies were noted in patients with SLE compared to healthy controls. 17 Certain studies have evaluated the potential role of medications in mediating lymphoma risk in SLE. A case-cohort analysis of a multicenter international SLE cohort suggested an increased risk of lymphoma in subjects exposed to cyclophosphamide as well as to cumulative glucocorticosteroids compared to SLE controls without cancer.…”

Late-onset systemic lupus erythematosus in the elderly

“…Отмечаются увеличение ри-ска развития неходжкинской лимфомы, рака легких, пече-ни, шейки матки и щитовидной железы и снижение часто-ты рака молочной железы и простаты по сравнению с ана-логичными показателями в популяции. Высказывается предположение, что лимфопролиферативные заболевания обусловлены повышенной активностью провоспалитель-ных цитокинов и, возможно, сопутствующей вирусной ин-фекцией (вирус Эпштейна-Барр), цитотоксической тера-пией (особенно экспозицией циклофосфамида), тогда как снижение частоты гормонально-зависимых опухолей (мо-лочной и предстательной желез) связано с наличием аутоан-тител и снижением выработки некоторых белков при СКВ (например, heat shock protein 27, HSP-27) [35][36][37][38]. Однако убедительных данных эпидемиологических исследований об ассоциации СКВ со злокачественными новообразовани-ями, в том числе в зависимости от возраста дебюта и прово-димой терапии, не получено.…”

The sero-epidemiology of infectious mononucleosis in Neyshabur, Northeast Iran during 2010–2014

“…Some individuals are more vulnerable than others to develop clinical symptoms from delayed infection, while there is no reason [5,6]. CD8 + T cells play a key protective role for the control of latent EBV infection.…”