Molecular Mimicry and Autoimmunity

Maoz-Segal, Ramit; Andrade, Paulo

doi:10.1016/b978-0-444-63269-2.00054-4

Cited by 4 publications

(1 citation statement)

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“…The Papillomaviridae family encompasses over 150 HPV subtypes, with types 16 and 18 being primary culprits in cervical cancers [11]. Molecular mimicry has been implicated in various autoimmune conditions, including rheumatoid arthritis, systemic lupus erythematosus (SLE), Sjogren's syndrome, autoimmune liver disease, inflammatory bowel disease, and multiple sclerosis [12]. This phenomenon has also been proposed to explain the rare occurrences of autoimmune disease activation or flares following vaccination; however, such data are scarce and sometimes conflicting, necessitating cautious interpretation to avoid potential confounders or the mistaken extrapolation of correlation for causation [13][14][15][16].…”

Section: Discussionmentioning

confidence: 99%

A Novel Association Between Human Papillomavirus and Thyroid Eye Disease

Garg,

Meyer,

Gallo

et al. 2024

Preprint

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Context: Thyroid eye disease (TED) is an autoimmune disease characterized by orbital inflammation and tissue remodeling. TED pathogenesis is poorly understood but is linked to autoantibodies to thyroid-stimulating hormone receptor (TSHR) and insulin-like growth factor 1 receptor (IGF-1R). Objective: To explore the potential involvement of viral infections in TED pathogenesis. Methods: Using NCBI BLAST, we compared human TSHR and IGF-1R proteins to various viral proteomes, including Papillomaviridae, Paramyxoviridae, Herpesviridae, Enterovirus, Polyomaviridae, and Rhabdoviridae. Enzyme-linked immunoassays (ELISAs) were performed on orbital adipose tissue samples from 22 TED patients and controls to quantify antiviral antibody titers. Demographics and clinical data were reviewed. Results: Homology analysis revealed conserved motifs between TSHR and IGF-1R with several viral proteins, particularly the human papillomavirus 18 (HPV18) L1 capsid protein. Basic demographic and clinical information between the cohorts were comparable. ELISAs showed statistically significant differences in the average HPV18 L1 IgG normalized optical density levels among tissues of control (M = 0.9387, SD = 0.3548), chronic TED (M = 2.305, SD = 1.064), and active acute TED (M = 4.087, SD = 2.034) patients. These elevated HPV18 L1 IgG titers did not statistically correlate with TSH, T4, or TSI levels, and were elevated in TED patients irrespective of treatment with teprotumumab, indicating a direct immunological response to HPV. Conclusions: This study presents the first molecular evidence linking HPV and TED, highlighting molecular mimicry between HPV capsid protein and key autoimmunity targets in TED. This suggests an immunological link contributing to TED's pathogenesis, opening new avenues for understanding and managing the disease.

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Section: Discussionmentioning

confidence: 99%