DescriptionAward: Best oral presentation in the session "Free Communications: Pearls in Autoimmunity"
Background and aims. Studies have linked HHV-6 with thyroid autoimmunity, yet the exact mechanisms of HHV-6 involvement remain unclear. We propose that two poorly studied HHV-6 proteins – U12 and U51, may contribute to autoimmunity. They are homologous to chemokine receptors (G-protein coupled receptors), can be expressed on cell surfaces, and can influence viral replication. By conducting molecular and immunological investigations, we aim to elucidate the potential role of U12/U51 in thyroid autoimmunity.
Methods. Thyroid tissue and plasma samples from 54 AIT patients (harboring HHV-6 in the thyroid) were investigated. RNA was isolated from thyroid tissues, used for cDNA synthesis, and nPCR to detect U12, U51 mRNA. FFPE thyroid tissues were microscoped to visualize U12/U51. U12 and U51 antibodies were detected with the Luminex system.
Results. 44% of thyroid tissues harbored U12/U51 mRNA. Thyroid tissues with mRNA harbored significantly higher viral loads (1998 vs 2038 viral copies/106 cells, p Conclusions. The combination of the presence of U12/U51 mRNA and viral protein-specific antibodies with the visualization of both HHV-6 and its GPCRs in the thyroid suggests that both could be involved in autoimmunity development/exacerbation. HHV-6 and U12/U51 could enhance thyroid cell destruction, autoantigen release, and inflammation through viral replication enhancement or through direct antibody binding and subsequent immune response against U12/U51.
|Period||17 Mar 2023|
|Event title||7th International Congress on Controversies in Rheumatology & Autoimmunity|
|Location||Turin, ItalyShow on map|
|Degree of Recognition||International|
Documents & Links
- Certificate Best Oral Presenation
File: application/pdf, 6.96 MB