Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link?



Nicola Tugnet*, 1, Paul Rylance 2, Denise Roden 3, Malgorzata Trela 3, Paul Nelson 3
1 Department of Rheumatology, Royal Wolverhampton Hospitals NHS Trust, Wolverhampton, UK
2 Department of Nephrology, Royal Wolverhampton Hospitals NHS Trust, Wolverhampton, UK
3 Molecular Immunology Research Group, Research Institute in Healthcare Science, University of Wolverhampton, UK


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© Tugnet et al.; Licensee Bentham Open.

open-access license: This is an open access article licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

* Address correspondence to this author at the Department of Rheumatology, New Cross Hospital, Wednesfield Road, Wolverhampton, WV10 0QP, UK; Tel: (+44) 1902 695492; Fax: (+44) 1902 695736; E-mail: ntugnet@doctors.org.uk


Abstract

Autoimmune rheumatic diseases, such as RA and SLE, are caused by genetic, hormonal and environmental factors. Human Endogenous Retroviruses (HERVs) may be triggers of autoimmune rheumatic disease. HERVs are fossil viruses that began to be integrated into the human genome some 30-40 million years ago and now make up 8% of the genome. Evidence suggests HERVs may cause RA and SLE, among other rheumatic diseases. The key mechanisms by which HERVS are postulated to cause disease include molecular mimicry and immune dysregulation. Identification of HERVs in RA and SLE could lead to novel treatments for these chronic conditions. This review summarises the evidence for HERVs as contributors to autoimmune rheumatic disease and the clinical implications and mechanisms of pathogenesis are discussed.

Keywords: Human endogenous retrovirus, HERV, rheumatoid arthritis, molecular mimicry, bioinformatics..