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Updated: Nov 16, 2025

Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions

Infection of Primary Nasal Epithelial Cells Grown at an Air-Liquid Interface to Characterize Human Coronavirus-Host Interactions

Published on: September 22, 2023

SARS-CoV-2 causes severe epithelial inflammation and barrier dysfunction.

Stefanie Deinhardt-Emmer¹, Sarah Böttcher², Clio Häring²

¹Institute of Medical Microbiology, Jena University Hospital, Am Klinikum 1, D-07747 Jena, Germany stefanie.deinhardt-emmer@med.uni-jena.de Christina.Ehrhardt@med.uni-jena.de.

Journal of Virology

|February 27, 2021

Summary

Severe coronavirus disease-19 (COVID-19) involves barrier damage. This study shows SARS-CoV-2 infects lung epithelial cells, not endothelial cells, but damages the epithelial-endothelial barrier, promoting viral spread.

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Published on: November 22, 2024

Area of Science:

Virology
Cell Biology
Pathogen-Host Interactions

Background:

SARS-CoV-2 causes COVID-19 with varying severity, sometimes involving systemic symptoms.
The mechanism by which SARS-CoV-2 breaches the alveolar barrier in severe COVID-19 remains unclear.
Understanding molecular pathogen-host interactions is crucial for developing effective countermeasures.

Purpose of the Study:

To investigate the effects of SARS-CoV-2 on epithelial and endothelial barrier integrity.
To elucidate the immune responses and viral dissemination pathways in a human chip model.
To determine the role of endothelial cells in SARS-CoV-2 infection.

Main Methods:

Utilized mono-cell culture systems and a complex human chip model with epithelial, endothelial, and mononuclear cells.
Assessed SARS-CoV-2 infection, viral load, and inflammatory responses in different cell types.
Evaluated barrier integrity and function over the course of infection.

Main Results:

SARS-CoV-2 efficiently infected epithelial cells, inducing high viral loads and inflammatory responses, including interferon production.
The adjacent endothelial layer showed no productive viral replication or interferon release.
Prolonged infection led to damage in both cell types, deteriorating barrier function and enabling viral spread.

Conclusions:

SARS-CoV-2 replication is dependent on epithelial cells, but infection impacts neighboring endothelial cells indirectly.
Virus-induced host factors, not direct infection, disrupt the epithelial-endothelial barrier.
This disruption facilitates viral dissemination and may explain links to thromboembolic events in severe COVID-19.