Relationship between Hepatitis C Virus Infection and Iron Overload

Chin Med J (Engl). 2017 Apr 5;130(7):866-871. doi: 10.4103/0366-6999.202737.


Objective: The aim of this study was to summarize the interactions between hepatitis C virus (HCV) infection and iron overload, and to understand the mechanisms of iron overload in chronic hepatitis C (CHC) and the role iron plays in HCV life cycle.

Data sources: This review was based on data in articles published in the PubMed databases up to January 28, 2017, with the keywords "hepatitis C virus", "iron overload", "iron metabolism", "hepcidin", "translation", and "replication".

Study selection: Articles related to iron metabolism, iron overload in patients with CHC, or the effects of iron on HCV life cycle were selected for the review.

Results: Iron overload is common in patients with CHC. The mechanisms involve decreased hepcidin levels caused by HCV through signal transducer and activator of transcription 3, mitogen-activated protein kinase, or bone morphogenetic protein/SMAD signaling pathways, and the altered expression of other iron-metabolism-related genes. Some studies found that iron increases HCV replication, while other studies found the opposite result. Most of the studies suggest the positive role of iron on HCV translation, the mechanisms of which involve increased expression levels of factors associated with HCV internal ribosome entry site-dependent translation, such as eukaryotic initiation factor 3 and La protein.

Conclusion: The growing literature demonstrates that CHC leads to iron overload, and iron affects the HCV life cycle in turn. Further research should be conducted to clarify the mechanism involved in the complicated interaction between iron and HCV.

Publication types

  • Review

MeSH terms

  • Female
  • Hepacivirus / pathogenicity
  • Hepatitis C / complications*
  • Hepatitis C / metabolism
  • Hepcidins / metabolism
  • Humans
  • Iron Overload / etiology*
  • Iron Overload / metabolism
  • Iron Overload / virology*
  • Male
  • Signal Transduction


  • Hepcidins