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. 2013 Mar 22:7:13-21.
doi: 10.2174/1874312901307010013. Print 2013.

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

Nicola Tugnet  1 , Paul Rylance, Denise Roden, Malgorzata Trela, Paul Nelson
Affiliations

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

Nicola Tugnet et al. Open Rheumatol J. .

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: HERV; Human endogenous retrovirus; bioinformatics.; molecular mimicry; rheumatoid arthritis.

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Figures

Fig. (1)
Fig. (1)
Structure of human endogenous retroviruses (HERVs). HERV products may be generated using different open reading frames (ORFs)
Fig. (2)
Fig. (2)
Molecular models of HERV-K10/IgG1Fc epitopes. Epitopes A and B taken from Westwood [18] and modeled using PyMOL (Molecular Graphics System, Version 1.2r3pre, Schrodinger, LLC: http://www.pymol.org/pymol) and enhanced using UCSF Chimera (http://www.cgl.ucsf.edu/chimera). Molecular models were displayed in ‘mesh’ mode. Arrows point to amino acid residues highlighted and displayed on an IgGFc molecule (PDB file: 3AVE) using UCSF Chimera. CH: constant heavy 2 and 3 domains of IgG. In B: despite the amino acid substitution, there appears to be little change in molecular shape which may facilitate antibody cross-reactivity.
Fig. (3)
Fig. (3)
Schematic interactions with human endogenous retroviruses. The interaction of HERVs on the immune system may be complex, compounded by external and internal factors to augment detrimental effects at the molecular and protein level.
See this image and copyright information in PMC

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