PMC:7289100 / 43-1790
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7289100","sourcedb":"PMC","sourceid":"7289100","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7289100","text":"Though the exact etiology of autoimmune diseases still remains unknown, there are various factors which are believed to contribute to the emergence of an autoimmune disease in a host including the genetic predisposition, the environmental triggers such as bacterial infections, including the gut microbiota, viral fungal and parasitic infections, as well as physical and environmental agents, hormonal factors and the hosts immune system dysregulation. All these factors interplay was coined by Shoenfeld et al., many years ago “The Mosaic of Autoimmunity” [[1], [2], [3], [4]]. The most prominent pathogenic viruses which have been proposed in the triggering and initiation of autoimmune diseases include: Parvovirus B19, Epstein-Barr-virus (EBV), Cytomegalovirus (CMV), Herpes virus-6, HTLV-1, Hepatitis A and C virus, and Rubella virus [[5], [6], [7], [8], [9], [10], [11]]. These viruses have been implicated in the initiation of chronic inflammatory or autoimmune diseases such as rheumatoid arthritis, systemic lupus erythematosus, Sjogren's syndrome, primary billiary cholangitis, multiple sclerosis, polymoysitis, uveitis, Henoch Schonlein Puprpura, Systemic Juvenile Idiopathic arthritis, systemic sclerosis, Hashimoto thyroiditis and autoimmune hepatitis [12,13]. Suggested mechanisms of induction of the autoimmunity include both molecular mimicry [14] as well as “bystander activation” whereby the infection may lead to activation of antigen presenting cells that may in turn activate pre-primed auto-reactive T-cells, thus leading to the production of pro-inflammatory mediators, which in turn may lead to tissue damage [15]. Alternative suggested mechanisms include epitope spreading as well as presentation of cryptic antigens 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