RT Journal Article SR Electronic T1 Rheumatoid Arthritis is Associated with IgG Antibodies to Human Endogenous Retrovirus Gag Matrix: A Potential Pathogenic Mechanism of Disease? JF The Journal of Rheumatology JO J Rheumatol FD The Journal of Rheumatology SP 1952 OP 1960 DO 10.3899/jrheum.130502 VO 41 IS 10 A1 Paul N. Nelson A1 Denise Roden A1 Alan Nevill A1 Graham L. Freimanis A1 Malgorzata Trela A1 Hora Davari Ejtehadi A1 Simon Bowman A1 John Axford A1 Andy M. Veitch A1 Nicola Tugnet A1 Paul B. Rylance YR 2014 UL http://www.jrheum.org/content/41/10/1952.abstract AB Objective. Human endogenous retrovirus (HERV)-K10 has been implicated in the etiology and pathogenesis of rheumatoid arthritis (RA). A secondary immune response to this virus might suggest an antigen-driven response in patients. The Gag region of HERV-K10 could provide a key epitope important for immunological reactivity. We investigated the presence of IgG antibodies to this region and assessed its significance in RA. Methods. We determined an antigenic peptide on the matrix segment of HERV-K10 and developed an ELISA system to detect IgG antibodies in patients with RA and controls. The presence of antibodies to the matrix peptide (denoted as MAG1: RIGKELKQAGRKGNI) was correlated with patient details. Results. On screening patients’ serum, we found a significantly higher mean IgG antibody response to MAG1 in 30 patients with RA as compared to 23 patients with inflammatory bowel disease (p = 0.003), 29 patients with osteoarthritis (p = 0.001), and 43 healthy individuals (p = 0.002). Reactivity was not observed to a control peptide possessing a nonhomologous amino acid sequence. On evaluating clinical details with serological activity, no correlation with disease duration (p = 0.128), sex (p = 0.768), or rheumatoid factor status (p = 0.576) was found. Conclusion. A significantly elevated IgG antibody response to an HERV-K10 Gag matrix peptide was observed in patients with RA, suggesting that the exposure of HERV-K10 may cause a secondary, antigenic driven immune response in RA.