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Commentary
Stem cell-derived HCV infection systems illustrate the bright future of human hepatocyte research
  1. Ype P de Jong1,2,
  2. T Jake Liang3
  1. 1 Division of Gastroenterology and Hepatology, Weill Cornell Medicine, New York, New York, USA
  2. 2 Laboratory of Virology and Infectious Disease, The Rockefeller University, New York, New York, USA
  3. 3 Liver Diseases Branch, NIDDK, National Institutes of Health, Bethesda, Maryland, USA
  1. Correspondence to Dr Ype P de Jong; ydj2001{at}med.cornell.edu; Dr T Jake Liang; jakel{at}bdg10.niddk.nih.gov

https://doi.org/10.1136/gutjnl-2020-321216

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    Most cells in the body can produce the cytokine interferon (IFN) in response to viral infections. IFN produced by virus-infected cell signals in both autocrine and paracrine fashion through the janus kinase/signal transducer and activator of transcription (Jak/STAT) pathway to activate interferon stimulated genes (ISG). There are over 400 ISG with numerous antiviral functions. Depending on the virus and the cell type, subsets of ISG are induced that help clear the infection. Thus, the IFN-ISG pathways are complex networks that form the first response to viral infections.1

    For many decades, chronic hepatitis C virus (HCV) infection was the leading cause of advanced liver disease in many nations around the world. Exposure to HCV leads to spontaneous clearance in 20%–30% of individuals, while the majority develop chronic infection that can lead to advanced liver disease. On exposure to HCV, human livers respond by producing a number of ISG. Based on several observations, ISGs have long been postulated to play a key role in HCV clearance. Since the early 1990s high doses of recombinant IFNα became the first effective treatment for HCV infection. For over two decades, various formulations of IFNα remained …

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    Footnotes

    • Contributors Both authors equally conceived, composed, reviewed and finalised the submitted articles.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

    • Patient consent for publication Not required.

    • Provenance and peer review Commissioned; internally peer reviewed.

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