Molecular mimicry, bystander activation, or viral persistence: infections and autoimmune disease.
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 persistence. 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.
Fujinami
Robert S
RS
Department of Neurology, University of Utah School of Medicine, 30 N 1900 E, 3R330 SOM, Salt Lake City, UT 84132-2305, USA. Robert.Fujinami@hsc.utah.edu
von Herrath
Matthias G
MG
Christen
Urs
U
Whitton
J Lindsay
JL
D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology* / Q000276:immunology*; D024201:Bystander Effect / Q000276:immunology*; D005260:Female; D006801:Humans; D008213:Lymphocyte Activation; D051379:Mice; D018716:Molecular Mimicry / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D014777:Virus Diseases / Q000150:complications*; D014780:Viruses / Q000254:growth & development