Increase in Human Endogenous Retrovirus HERV-K (HML-2) Viral Load in Active Rheumatoid Arthritis

Authors

  • F. Reynier,

    1. Joint Unit Hospices Civils de Lyon – bioMérieux, and Department of Immunology and Rheumatology, Immunogenomics and inflammation research Unit EA 4130, University of Lyon, Edouard Herriot Hospital, Lyon, France
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  • T. Verjat,

    1. Biomarker research and validation Department – Centre Christophe Mérieux, bioMérieux SA, Grenoble, France
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  • F. Turrel,

    1. Joint Unit Hospices Civils de Lyon – bioMérieux, and Department of Immunology and Rheumatology, Immunogenomics and inflammation research Unit EA 4130, University of Lyon, Edouard Herriot Hospital, Lyon, France
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  • P. E. Imbert,

    1. Joint Unit Hospices Civils de Lyon – bioMérieux, and Department of Immunology and Rheumatology, Immunogenomics and inflammation research Unit EA 4130, University of Lyon, Edouard Herriot Hospital, Lyon, France
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  • H. Marotte,

    1. Joint Unit Hospices Civils de Lyon – bioMérieux, and Department of Immunology and Rheumatology, Immunogenomics and inflammation research Unit EA 4130, University of Lyon, Edouard Herriot Hospital, Lyon, France
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  • B. Mougin,

    1. Joint Unit Hospices Civils de Lyon – bioMérieux, and Department of Immunology and Rheumatology, Immunogenomics and inflammation research Unit EA 4130, University of Lyon, Edouard Herriot Hospital, Lyon, France
    2. Biomarker research and validation Department – Centre Christophe Mérieux, bioMérieux SA, Grenoble, France
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  • P. Miossec

    1. Joint Unit Hospices Civils de Lyon – bioMérieux, and Department of Immunology and Rheumatology, Immunogenomics and inflammation research Unit EA 4130, University of Lyon, Edouard Herriot Hospital, Lyon, France
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Professor P. Miossec, Clinical Immunology Unit, Departments of Immunology and Rheumatology, Hôpital Edouard Herriot, 69437 Lyon Cedex 03, France. E-mail: miossec@univ-lyon1.fr

Abstract

To study the viral loads of human endogenous retrovirus HERV-K (HML-2) type 1 and type 2 in rheumatoid arthritis (RA), we measured the viral loads of HERV-K (HML-2) type 1 and type 2 using nucleic acid sequence-based amplification (NASBA) technology. We analyzed plasma samples from RA patients (n = 79) and healthy volunteers (HV, n = 46) and synovial fluid samples from RA (n = 10) and osteoarthritis (OA, n = 10) patients. HERV-K type 1 and type 2 viruses were detected and quantified for the majority of plasma and synovial fluid samples from RA patients. HERV-K type 1 and type 2 viral loads were significantly elevated in RA patients compared with HV in plasma (P < 0.0001) and from RA patients compared with OA patients in synovial fluid (type 1: P = 0.0007; type 2: P = 0.023). Moreover, an association was observed between the HERV-K type 1 viral load in plasma and the disease activity in RA patients (RA patients with low activity versus high activity P = 0.0129; RA patients with intermediate activity versus high activity P = 0.037). Our findings showed that HERV-K (HML-2) viral load can be detected in plasma samples from RA patients, with higher levels observed for those with active disease. There was an association of HERV-K type 1 levels with the disease activity.

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