Abstract

Introduction: The mechanisms by which hepatitis C virus (HCV) infection induces autoimmune thyroiditis (AIT) have been studied, and it was suggested that inflammatory cytokines during HCV infection would change the thyroperoxidase (TPO) signaling cascade and thyroglobulin (Tg) determining autoimmune thyroid disease.Objective: To show the signaling pathway, of TPO and Tg, and their potential targets mediated HCV in individuals with hepatitis C.Methods: The mapping of the signaling pathway was based on a review study approach and performed using the automatic annotation server of the Kyoto and Genome Encyclopedia (KEGG). PathVisio is free software for analysis and design of open source routes, and was used for the graphic representation of the signaling pathway.Results: The contigs were extracted from the KEGG database and their mapped transcription represents the signaling pathway of the main biomolecules that triggers the AIT. The action of HCV, or its treatment can trigger AIT that is characterized by the presence of autoantibodies against TPO and Tg. In AIT, autoreactive CD4 + T lymphocytes recruit B cells and CD8 + T cells in the thyroid. The progression of the disease leads to the death of thyroid cellsand hypothyroidism.Conclusion: HCV or its treatment activates several signaling pathways with thyroid cells damage resulting in AIT and secondary hypothyroidism to cellular apoptosis.

Highlights

  • The mechanisms by which hepatitis C virus (HCV) infection induces autoimmune thyroiditis (AIT) have been studied, and it was suggested that inflammatory cytokines during HCV infection would change the thyroperoxidase (TPO) signaling cascade and thyroglobulin (Tg) determining autoimmune thyroid disease

  • We show the signaling pathway of TPO and Tg, and their potential targets for the HCV-mediated AIT based on a review of the literature

  • It has been hypothesized that individuals with genetic susceptibility for AIT exposed to HCV infection may develop thyroiditis

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Summary

Introduction

The mechanisms by which hepatitis C virus (HCV) infection induces autoimmune thyroiditis (AIT) have been studied, and it was suggested that inflammatory cytokines during HCV infection would change the thyroperoxidase (TPO) signaling cascade and thyroglobulin (Tg) determining autoimmune thyroid disease. Conclusion: HCV or its treatment activates several signaling pathways with thyroid cells damage resulting in AIT and secondary hypothyroidism to cellular apoptosis. The hepatitis C virus (HCV) infection is associated to endocrine-metabolic disorders including AIT.[4] Studies have shown that the therapy for HCV induces thyroid diseases, and female sex, positive TPO-Ab and elevated serum of thyroid-stimulating hormone (TSH) concentration are important risk factors for AIT development.[5] It has been suggested that the elevation of interleukins (IL) in inflammation caused by HCV would alter the signaling cascade of TPO and Tg determining autoimmune thyroid disease.[6]

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