Epstein-Barr Virus in Systemic Autoimmune DiseasesReport as inadecuate




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Clinical and Developmental ImmunologyVolume 2013 2013, Article ID 535738, 9 pages

Review ArticleDepartment of Clinical Biochemistry, Immunology and Genetics, Statens Serum Institut, Artillerivej 5, 2300 Copenhagen, Denmark

Received 24 May 2013; Accepted 17 July 2013

Academic Editor: Guixiu Shi

Copyright © 2013 Anette Holck Draborg et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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.





Author: Anette Holck Draborg, Karen Duus, and Gunnar Houen

Source: https://www.hindawi.com/



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