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

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...

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Autores principales: Tugnet, Nicola, Rylance, Paul, Roden, Denise, Trela, Malgorzata, Nelson, Paul
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Bentham Open 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3636489/
https://www.ncbi.nlm.nih.gov/pubmed/23750183
http://dx.doi.org/10.2174/1874312901307010013
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author Tugnet, Nicola
Rylance, Paul
Roden, Denise
Trela, Malgorzata
Nelson, Paul
author_facet Tugnet, Nicola
Rylance, Paul
Roden, Denise
Trela, Malgorzata
Nelson, Paul
author_sort Tugnet, Nicola
collection PubMed
description 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.
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spelling pubmed-36364892013-06-07 Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link? Tugnet, Nicola Rylance, Paul Roden, Denise Trela, Malgorzata Nelson, Paul Open Rheumatol J Article 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. Bentham Open 2013-03-22 /pmc/articles/PMC3636489/ /pubmed/23750183 http://dx.doi.org/10.2174/1874312901307010013 Text en © Tugnet et al.; Licensee Bentham Open. http://creativecommons.org/licenses/by-nc/3.0/ 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.
spellingShingle Article
Tugnet, Nicola
Rylance, Paul
Roden, Denise
Trela, Malgorzata
Nelson, Paul
Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link?
title Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link?
title_full Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link?
title_fullStr Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link?
title_full_unstemmed Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link?
title_short Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link?
title_sort human endogenous retroviruses (hervs) and autoimmune rheumatic disease: is there a link?
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3636489/
https://www.ncbi.nlm.nih.gov/pubmed/23750183
http://dx.doi.org/10.2174/1874312901307010013
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