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Research Article Free access | 10.1172/JCI119856

An increased prevalence of Epstein-Barr virus infection in young patients suggests a possible etiology for systemic lupus erythematosus.

J A James, K M Kaufman, A D Farris, E Taylor-Albert, T J Lehman, and J B Harley

Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.

Find articles by James, J. in: PubMed | Google Scholar

Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.

Find articles by Kaufman, K. in: PubMed | Google Scholar

Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.

Find articles by Farris, A. in: PubMed | Google Scholar

Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.

Find articles by Taylor-Albert, E. in: PubMed | Google Scholar

Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.

Find articles by Lehman, T. in: PubMed | Google Scholar

Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 73104, USA.

Find articles by Harley, J. in: PubMed | Google Scholar

Published December 15, 1997 - More info

Published in Volume 100, Issue 12 on December 15, 1997
J Clin Invest. 1997;100(12):3019–3026. https://doi.org/10.1172/JCI119856.
© 1997 The American Society for Clinical Investigation
Published December 15, 1997 - Version history
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Abstract

An unknown environmental agent has been suspected to induce systemic lupus erythematosus (lupus) in man. Prompted by our recent immunochemical findings, we sought evidence for an association between Epstein-Barr virus infection and lupus. Because the vast majority of adults have been infected with Epstein-Barr virus, we chose to study children and young adults. Virtually all (116 of 117, or 99%) of these young patients had seroconverted against Epstein-Barr virus, as compared with only 70% (107 of 153) of their controls (odds ratio 49.9, 95% confidence interval 9.3-1025, P < 0. 00000000001). The difference in the rate of Epstein-Barr virus seroconversion could not be explained by serum IgG level or by cross-reacting anti-Sm/nRNP autoantibodies. No similar difference was found in the seroconversion rates against four other herpes viruses. An assay for Epstein-Barr viral DNA in peripheral blood lymphocytes established Epstein-Barr virus infection in the peripheral blood of all 32 of the lupus patients tested, while only 23 of the 32 matched controls were infected (odds ratio > 10, 95% confidence interval 2.53-infinity, P < 0.002). When considered with other evidence supporting a relationship between Epstein-Barr virus and lupus, these data are consistent with, but do not in themselves establish, Epstein-Barr virus infection as an etiologic factor in lupus.

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