Is Epstein–Barr virus reactivation associated with altered immune activity in people newly diagnosed with Hashimoto thyroiditis?

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Epstein–Barr virus (EBV) reactivation is increasingly recognized as a potential exacerbator of autoimmune diseases, including Hashimoto thyroiditis (HT). This study examined the association between EBV reactivation and intracellular Toll-like receptor (TLR) expression in newly diagnosed, untreated HT patients. Its aim was to investigate whether EBV reactivation and expression of TLR3, TLR7, TLR8, and TLR9 contribute to HT development and progression.

This observational cohort study compared 54 newly diagnosed, untreated HT patients with 20 healthy volunteers matched for age and sex. Blood samples were collected to assess EBV viral load and intracellular expression of TLR3, TLR7, TLR8, and TLR9; the abstract names flow cytometry in describing these assessments. Specific anti-EBV antibodies—viral capsid A (VCA) immunoglobulin M (IgM), VCA IgG, Epstein–Barr nuclear antigen 1 (EBNA-1) IgM, and EBNA-1 IgG—were measured to identify signs of EBV reactivation. Soluble receptors sTLR3, sTLR7, sTLR8, and sTLR9 were quantified in serum using enzyme-linked immunosorbent assay (ELISA). Notably, the HT patients were not euthyroid: compared with healthy volunteers, they had significantly lower thyroid-stimulating hormone levels and elevated free triiodothyronine and free thyroxine levels.

The study reported significantly increased EBV reactivation in the HT group: 26 of 54 patients (48.1%) tested positive for EBV DNA, compared with none of the healthy volunteers. HT patients with reactivated EBV showed significantly higher intracellular expression of TLR3, TLR7, and TLR9. TLR3-positive cells made up an average of 4.72% of CD4-positive lymphocytes, compared with 0.69% in healthy volunteers, suggesting a potential synergistic effect. Soluble TLR levels also increased in HT patients with reactivated EBV, suggesting a possible role for these receptors in amplifying autoimmune responses.

The researchers concluded that both viral reactivation and TLR activity should be considered in HT treatment. Understanding the interplay between EBV and intracellular TLRs may lead to new therapeutic approaches to reduce these factors’ impact on disease progression. Further research is needed to investigate the mechanisms underlying this interaction and its implications for treatment strategies.