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Clinical Microbiology Reviews, January 2006, p. 80-94, Vol. 19, No. 1
0893-8512/06/$08.00+0     doi:10.1128/CMR.19.1.80-94.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease

Robert S. Fujinami,1* Matthias G. von Herrath,2 Urs Christen,2 and J. Lindsay Whitton3

Department of Neurology, University of Utah School of Medicine, Salt Lake City, Utah 84132-2305,1 Division of Immune Regulation, La Jolla Institute for Allergy and Immunology, San Diego, California 92121,2 Department of Neuropharmacology, The Scripps Research Institute, La Jolla, California 920373

Virus infections and autoimmune disease have long been linked. These infections often precede the occurrence of inflammation in the target organ. Several mechanisms often used to explain the association of autoimmunity and virus infection are molecular mimicry, bystander activation (with or without epitope spreading), and viral persistance. These mechanisms have been used separately or in various combinations to account for the immunopathology observed at the site of infection and/or sites of autoimmune disease, such as the brain, heart, and pancreas. These mechanisms are discussed in the context of multiple sclerosis, myocarditis, and diabetes, three immune-medicated diseases often linked with virus infections.

* Corresponding author. Mailing address: Department of Neurology, University of Utah School of Medicine, 30 N 1900 E, 3R330 SOM, Salt Lake City, UT 84132-2305. Phone: (801) 585-3305. Fax: (801) 585-3311. E-mail: Robert.Fujinami{at}hsc.utah.edu.

Clinical Microbiology Reviews, January 2006, p. 80-94, Vol. 19, No. 1
0893-8512/06/$08.00+0     doi:10.1128/CMR.19.1.80-94.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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Antimicrob. Agents Chemother. Clin. Vaccine Immunol.
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Copyright © 2006 by the American Society for Microbiology. All rights reserved.