Endocrine-immune interactions in Hashimoto’s thyroiditis and human papillomavirus-induced cervical cancer: The role of Epstein-Barr, hepatitis C, and hepatitis D viruses in shared pathogenesis
TL;DR
Current evidence remains insufficient to confirm a direct association between HT and an increased risk of developing CC, and further experimental and epidemiological studies are required to elucidate the potential relationship between HT and HPV-induced CC.
Abstract
Hashimoto’s thyroiditis (HT) and human papillomavirus (HPV)-induced cervical cancer (CC) are distinct clinical entities; however, their etiologies share several pathogenetic mechanisms related to immune dysregulation, endocrine disturbances, and chronic inflammation. HT is an autoimmune disease characterized by lymphocytic infiltration of the thyroid gland, autoantibody production, and progressive tissue damage resulting from a persistent inflammatory response. In contrast, the development of HPV-induced CC depends on the virus’s ability to evade host immune surveillance, thereby enabling long-term persistence of the infection. Increasing evidence suggests a potential role of other viral infections, particularly Epstein-Barr virus and hepatitis C virus, in the development of autoimmune thyroid diseases. The underlying mechanisms include chronic inflammation, molecular mimicry, and impaired immune tolerance. Furthermore, thyroid hormones and the sex hormones estrogen and progesterone play a significant role in modulating innate and adaptive immune responses and may influence the persistence of viral infections. Although there is an overlap in the immunological and endocrine mechanisms involved in these conditions, current evidence remains insufficient to confirm a direct association between HT and an increased risk of developing CC. Further experimental and epidemiological studies are required to elucidate the potential relationship between HT and HPV-induced CC.