TY - JOUR T1 - Human herpesvirus 6A active infection in patients with autoimmune Hashimoto's thyroiditis JO - The Brazilian Journal of Infectious Diseases T2 - AU - Seyyedi,Noorossadat AU - Dehbidi,Gholamreza Rafiei AU - Karimi,Mozhgan AU - Asgari,Amir AU - Esmaeili,Babak AU - Zare,Farahnaz AU - Farhadi,Ali AU - Dabbaghmanesh,Mohammad Hossein AU - Saki,Forough AU - Behzad-Behbahani,Abbas SN - 14138670 M3 - 10.1016/j.bjid.2019.10.004 DO - 10.1016/j.bjid.2019.10.004 UR - https://www.bjid.org.br/en-human-herpesvirus-6a-active-infection-articulo-S1413867019304635 AB - BackgroundHypothyroidism due to Hashimoto's thyroiditis (HT) is the commonest autoimmune endocrine illness in which antibodies against thyroid organ result in inflammation. The disease has a complex etiology that involves genetic and environmental influences. Viral infections may be involved in triggering of the disease as their molecular mimicry enhance autoimmune responses. Human herpesvirus-6 (HHV-6) is recognized for its contribution to some autoimmune diseases. ObjectiveIn the current study, the prevalence of HHV-6 active infection in patients with HT and with non-autoimmune thyroid disorders were compared with patients with euthyroidism. In addition, a correlation between presence of HHV-6 infections and HT was investigated. MethodsA total of 151 patients with clinically and laboratory confirmed HT, 59 patients with non-autoimmune thyroid disorders, and 32 patients with normal thyroid function were included in the study. For further confirmation of HT disease, all the precipitants were tested for anti-thyroid peroxidase (TPO), and anti-thyroglobulin (TG) antibodies. For detection of both HHV-6 types A and B, nested PCR and restriction enzyme digestion were used. HHV-6 DNA positive samples were further investigated by DNA sequencing analysis. ResultsHHV-6A DNA was found in serum sample of 57 out of 151 patients (38%) with HT, which was significantly more often than in patients with non-autoimmune thyroid disorders (p=0.001). However, HHV-6 DNA was not detected in serum samples of euthyroid subjects. ConclusionsThe results support a possible role for active HHV-6A infection, demonstrated by the presence of HHV-6 DNA in sera, in the development of HT. ER -