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Related Experiment Video

Updated: May 7, 2025

Live Imaging and Quantification of Viral Infection in K18 hACE2 Transgenic Mice Using Reporter-Expressing Recombinant SARS-CoV-2

Live Imaging and Quantification of Viral Infection in K18 hACE2 Transgenic Mice Using Reporter-Expressing Recombinant SARS-CoV-2

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SARS-CoV-2 Productively Infects Human Hepatocytes and Induces Cell Death.

Chunkyu Ko^1,2, Cho-Chin Cheng¹, Daniele Mistretta¹

¹Institute of Virology, Technical University of Munich/Helmholtz Munich, Munich, Germany.

Journal of Medical Virology

|January 6, 2025

Summary

This study reveals SARS-CoV-2 directly infects and replicates within human liver cells (hepatocytes), causing cell death and contributing to liver damage. This highlights the liver

Keywords:

ACE2 COVID‐19 SARS‐CoV‐2 TMPRSS2 hepatocytes liver tropism

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Area of Science:

Hepatology
Virology
Immunology

Background:

SARS-CoV-2 infection is linked to elevated liver enzymes.
Patients with pre-existing liver conditions face more severe COVID-19 outcomes.

Purpose of the Study:

To elucidate the mechanism of SARS-CoV-2 infection in human hepatocytes.
To demonstrate viral replication, spread, and direct hepatocyte damage.
To investigate the role of hepatocytes in SARS-CoV-2 pathogenesis.

Main Methods:

Infection of primary human hepatocytes and hepatoma cells with SARS-CoV-2 variants.
Knockdown of ACE2 and TMPRSS2 to assess infection pathways.
Electron microscopy to visualize viral particles.
Infection of C57BL/6 mice with a mouse-adapted SARS-CoV-2 strain.
Analysis of liver enzymes (ALT) and viral RNA levels.
Liver histology to evaluate tissue damage and immune response.

Main Results:

SARS-CoV-2 replicated efficiently in human hepatocytes and hepatoma cells across different variants.
Hepatocytes express ACE2 and TMPRSS2, crucial for viral entry.
Knockdown of ACE2/TMPRSS2 reduced SARS-CoV-2 infection.
Infected hepatocytes released infectious progeny viruses, indicating contribution to spread.
SARS-CoV-2 infection caused replication-dependent hepatocyte death.
Omicron variant showed faster onset but less cell death compared to others.
Infected mice exhibited high viral RNA in liver and lungs, with peak ALT during viral clearance.
Liver pathology showed significant damage and immune cell infiltration.

Conclusions:

Human hepatocytes are susceptible to SARS-CoV-2 infection, supporting viral replication and spread.
Direct cytopathic effects of SARS-CoV-2 on hepatocytes contribute to liver injury.
Immune-mediated killing of infected hepatocytes also plays a role in liver pathology during SARS-CoV-2 infection.