Amplification of autoimmune disease by infection

• Published in: Arthritis research & therapy Vol. 7; no. 2; pp. 74 - 84
• Main Authors: Posnett, David N, Yarilin, Dmitry
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 01.01.2005; BioMed Central
• Subjects: Animals; Antiviral Agents - administration & dosage; Antiviral Agents - therapeutic use; Autoimmune Diseases - complications; Autoimmune Diseases - immunology; Biological Transport; Chlamydia Infections - complications; Chlamydia Infections - immunology; Chlamydia Infections - prevention & control; Chlamydophila Infections - complications; Chlamydophila Infections - immunology; Chlamydophila Infections - prevention & control; Encephalomyelitis, Autoimmune, Experimental - complications; Encephalomyelitis, Autoimmune, Experimental - immunology; Herpesviridae Infections - complications; Herpesviridae Infections - immunology; Herpesviridae Infections - prevention & control; Humans; Immunocompromised Host; Immunosuppressive Agents - adverse effects; Immunosuppressive Agents - therapeutic use; Inflammation; Mice; Models, Immunological; Organ Specificity; Parvoviridae Infections - complications; Parvoviridae Infections - immunology; Parvoviridae Infections - prevention & control; Parvovirus B19, Human; Review; Rhadinovirus; Tumor Virus Infections - complications; Tumor Virus Infections - immunology; Viremia - complications; Viremia - immunology; Viremia - prevention & control; Virus Diseases - complications; Virus Diseases - immunology; Virus Diseases - prevention & control; Virus Replication
• ISSN: 1478-6354; 1478-6362
• DOI: 10.1186/ar1691

Reports of infection with certain chronic persistent microbes (herpesviruses or Chlamydiae) in human autoimmune diseases are consistent with the hypothesis that these microbes are reactivated in the setting of immunodeficiency and often target the site of autoimmune inflammation. New experimental animal models demonstrate the principle. A herpesvirus or Chlamydia species can be used to infect mice with induced transient autoimmune diseases. This results in increased disease severity and even relapse. The evidence suggests that the organisms are specifically imported to the inflammatory sites and cause further tissue destruction, especially when the host is immunosuppressed. We review the evidence for the amplification of autoimmune inflammatory disease by microbial infection, which may be a general mechanism applicable to many human diseases. We suggest that patients with autoimmune disorders receiving immunosuppressing drugs should benefit from preventive antiviral therapy.