ArticleThe Journal of clinical endocrinology and metabolism2020
Hepatitis C Virus Infection of Human Thyrocytes: Metabolic, Hormonal, and Immunological Implications.
Article in The Journal of clinical endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- Interplay Between Infectious Diseases and the Endocrine System: An Overview and Clinical Insights.Endocrinology, diabetes & metabolism · 2026Review
- Correlation between gynecomastia and endocrine regulation in patients with metabolic dysfunction-associated fatty liver disease: A cross-sectional study.World journal of hepatology · 2025Article
- Direct-acting antivirals used in HCV-related liver disease do not affect thyroid function and autoimmunity.Journal of endocrinological investigation · 2023Article
- Human T-cell leukemia virus type 1 is associated with dysthyroidism in the French Amazon.Frontiers in cellular and infection microbiology · 2023Article
- High Prevalence of Common Human Viruses in Thyroid Tissue.Frontiers in endocrinology · 2022Article
- Modulation of Production of Th1/Th2 Cytokines in Peripheral Blood Mononuclear Cells and Neutrophils by Hepatitis C Virus Infection in Chronically Infected Patients.Pathogens (Basel, Switzerland) · 2021Article
- HLA Class I Upregulation and Antiviral Immune Responses in Graves Disease.The Journal of clinical endocrinology and metabolism · 2021Article
- Assessing State Variation in Plastic Surgeons' Risk of Hepatitis C Exposure: Revisit in Methodology.Plastic and reconstructive surgery. Global open · 2020Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
contextHepatitis C virus (HCV) infection is a prevalent disease worldwide. Thyroid dysfunction is one of the most common extrahepatic manifestations of HCV infection. We hypothesized that HCV can directly infect human thyrocytes thereby causing thyroid dysfunction.
settingHuman thyrocytes in primary cell culture, ML-1 human thyroid cell line, and Huh7.5 human hepatocyte cell line were infected with HCV using the Huh7.5JFH1 cell line that releases infectious HCV virions. After infection, the release of new virions, production of proinflammatory cytokines, and expression of miR-122 were evaluated. Ribonucleic acid (RNA) extracted from HCV-infected cells and mock-infected cells was subjected to RNA sequencing and transcriptomic analysis. Ingenuity pathway analysis was used to detect up- and down-regulated pathways.
resultsHuman thyrocytes express major HCV entry factors including CD81, occludin, claudin-1, and scavenger receptor class B1. Viral infection of thyroid cells was confirmed by detection of HCV core protein in supernatants and negative-sense HCV RNA in cell lysates. HCV infection of thyrocytes induced the production of the chemokine CXCL-8 and the proinflammatory cytokines tumor necrosis factor alpha (TNF-α) and significantly increased the expression of miR-122. Moreover, HCV infection of thyrocytes decreased expression of the thyroid peroxidase and thyroglobulin genes and increased expression of the deiodinase 2 gene. The top upregulated pathways in HCV-infected thyrocytes were immune pathways and metabolic pathways, while infected hepatocytes upregulated lipid and glucose metabolism pathways as previously reported.
conclusionsHCV infection may induce thyroid dysfunction by different mechanisms including direct infection of thyrocytes leading to activation of inflammatory pathways and upregulation of miR-122. These findings support a general mechanism for viral induction of autoimmunity through direct infection of target tissues.
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