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Related Concept Videos

Hepatitis01:25

Hepatitis

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Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver.
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Stem cell-derived hepatocytes: A novel model for hepatitis E virus replication.

Nicky Helsen1, Yannick Debing2, Jan Paeshuyse2

  • 1Stem Cell Institute, University of Leuven (KU Leuven), Leuven, Belgium.

Journal of Hepatology
|December 3, 2015
PubMed
Summary
This summary is machine-generated.

Pluripotent stem cell-derived hepatocytes fully support hepatitis E virus (HEV) replication, offering a new model for studying HEV infection. Other stem cell derivatives support partial replication, highlighting early viral cycle steps as key to HEV tropism.

Keywords:
Cell culture modelHepatitis E virusHepatocytesPluripotent stem cells

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Area of Science:

  • Hepatology
  • Virology
  • Stem Cell Biology

Background:

  • Hepatitis E virus (HEV) causes millions of infections and tens of thousands of deaths annually.
  • While often self-limiting, HEV can lead to severe hepatitis, chronic infection, and fulminant liver failure.

Purpose of the Study:

  • To investigate if pluripotent stem cell (PSC)-derived hepatocytes, mesodermal cells, or neuroprogenitors support HEV replication.
  • To establish a novel in vitro model for studying HEV tropism and replication dynamics.

Main Methods:

  • Human PSCs were differentiated into hepatocyte-like cells, mesodermal cells, and neuroprogenitors.
  • Cells were infected with HEV and analyzed for viral RNA, infectious virions, and replication using qRT-PCR, in situ hybridization, and reporter assays.

Main Results:

  • PSC-derived hepatocytes supported the complete HEV replication cycle, including production of infectious virions.
  • HEV replication in PSC-hepatocytes was inhibited by ribavirin and interferon-α2b.
  • PSC-derived mesodermal and neuroprogenitor cells supported only partial HEV replication upon transfection with a subgenomic replicon.

Conclusions:

  • PSC-derived hepatocytes provide a physiologically relevant model to study HEV infection and replication.
  • The study demonstrates that early viral cycle steps are critical determinants of HEV tissue tropism.
  • This model may facilitate the development of new therapeutic strategies against HEV.