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Review
. 2016 Jan 18;8(2):83-91.
doi: 10.4254/wjh.v8.i2.83.

Hepatitis C virus infection and thyroid autoimmune disorders: A model of interactions between the host and the environment

Francesca Pastore  1 , Antonio Martocchia  1 , Manuela Stefanelli  1 , Pietro Prunas  1 , Stefania Giordano  1 , Lavinia Toussan  1 , Antonio Devito  1 , Paolo Falaschi  1
Affiliations
Review

Hepatitis C virus infection and thyroid autoimmune disorders: A model of interactions between the host and the environment

Francesca Pastore et al. World J Hepatol. .

Abstract

The hepatitis C virus (HCV) infection is an important public health problem and it is associated with hepatic and extrahepatic manifestations. Autoimmune thyroid diseases are common in HCV infected patients and the standard interferon-based treatment is associated with an increase of the immune-mediated thyroid damage. Recent evidence in the literature analyzed critical points of the mechanisms of thyroid damage, focusing on the balance between the two sides of the interaction: The environment (virus infection with potential cross-reaction) and the host (susceptibility genes with consistent immune response). The spectrum of antiviral treatment for chronic HCV infection is rapidly expanding for the development of dual o triple therapy. The availability of interferon-free combined treatment with direct antiviral agents for HCV is very promising, in order to ameliorate the patient compliance and to reduce the development of thyroid autoimmunity.

Keywords: Antiviral agents; Hepatitis C virus; Interferon; Self-tolerance; Thyroid autoimmunity.

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Figures

Figure 1
Figure 1
Potential mechanisms for self-tolerance control. AIRE: Autoimmune regulator gene; DCs: Dendritic cells; TGF: Transforming growth factor; IL: Interleukin; Ab: Antibody; NKT cells: Natural killer T cells.
Figure 2
Figure 2
Development of thyroid autoimmunity in patients with chronic hepatitis C virus infection during interferon-α treatment. Ab: Antibody; Ag: Antigen; APC: Antigen presenting cell; CD: Cluster of differentiation; CTLA-4: Cytotoxic T-lymphocyte antigen 4; CXCL10: C-X-C motif chemokine; DC: Dendritic cell; HCV: Hepatitis C virus; HLA: Human leukocyte antigen; I-: Iodide; IFN: Interferon; IL: Interleukin; NIS: Sodium/iodide symporter; PTPN22: Protein tyrosine phosphatase nonreceptor-type 22; T3 and T4: Thyroid hormones; TCR: T cell receptor; Tg: Thyroglobulin; TGF: Transforming growth factor; Th: T helper; TPO: Thyroid peroxidase; Tregs: T regulatory cells.
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