Does the Epstein-Barr Virus Play a Role in the Pathogenesis of Graves' Disease?

Graves' disease (GD) it the most common chronic organ-specific thyroid disorder without a fully recognized etiology. The pathogenesis of the disease accounts for an interaction between genetic, environmental, and immunological factors. The most important environmental factors include viral and bacterial infections. The Epstein-Barr virus (EBV) is one of the most common latent human viruses. Literature has suggested its role in the development of certain allergic and autoimmune diseases. EBV also exhibits oncogenic properties. The aim of the study was to analyze and compare the presence of EBV DNA in peripheral blood mononuclear cells (PBMCs) in patients with newly recognized GD and to find a correlation between EBV infection and the clinical picture of GD. The study included 39 untreated patients with newly diagnosed GD and a control group of 20 healthy volunteers who were gender and age matched. EBV DNA was detected with reverse transcription polymerase chain reaction (RT PCR) assay. The studies showed a significantly higher incidence of EBV copies in PBMCs among GD patients compared to the control group. Whereas, no significant correlations were found between the incidence of EBV copies and the evaluated clinical parameters. Our results suggest a probable role of EBV in GD development. EBV infection does not affect the clinical picture of Graves' disease.

Th17 and Treg cells in adolescents with Graves' disease. Impact of treatment with methimazole on these cell subsets.

The role of T helper 17 (Th17) and T regulatory cells (Treg) in the pathogenesis of Graves' disease (GD) remains uncertain. The influence of methimazole (MMI) on the human immune system is still poorly understood. The aim of the present research was to assess changes in the frequencies of peripheral blood Th17 and Treg cells during GD treatment in the group of teenagers. The frequencies of Th17 and Treg were measured by flow cytometry in 60 adolescents at the time of GD diagnosis and after achieving MMI-induced euthyreosis. The control group consisted of 20 healthy volunteers. Lower percentages and absolute counts of Treg cells were found in the study group before the treatment in comparison with healthy controls (p = 0.032 and p = 0.006, respectively). Treatment with MMI caused an increase in the percentages and absolute counts of Treg lymphocytes (p = 0.037 and p = 0.007). After the treatment, no clinically significant differences in Treg cells between GD patients and controls were found. Higher absolute counts of Th17 lymphocytes were found in hyperthyroid adolescents before the treatment initiation and after achieving euthyreosis than in healthy individuals (p = 0.0001 and p = 0.047). Treatment with MMI caused a significant decrease in the percentages and absolute counts of Th17 lymphocytes (p = 0.047 and p = 0.043). The present study demonstrates that both Th17 and Treg cells might play a role in the pathogenesis of GD. Increased percentage of Treg after MMI therapy seems a predictor of response to anti-hypertensive treatment as it is associated with the normalization of thyroid hormone levels.