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Updated: Jan 14, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

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Published on: June 3, 2018

Type I IFNs Decrease SARS-CoV-2 Replication in Human Cardiomyocytes and Increase Cytokine Production in Macrophages.

Verónica Durán^1,2,3, Eirini Nikolouli⁴, Shambhabi Chatterjee^5,6

¹Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture between the Helmholtz Centre for Infection Research [HZI], Braunschweig, and the Hannover Medical School [MHH], 30625, Hannover, Germany.

Journal of Clinical Immunology

|October 21, 2025

Summary

This summary is machine-generated.

Type I interferons reduce SARS-CoV-2 replication in human heart cells but enhance inflammatory responses in macrophages. This finding clarifies the role of interferon immunity in COVID-19 severity.

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High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

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High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes

Published on: March 24, 2015

Area of Science:

Immunology
Virology
Stem Cell Biology

Background:

The role of type I interferon (IFN) immunity in COVID-19 severity is not fully understood.
Investigating cellular responses to SARS-CoV-2 in patients with IFN deficiencies is crucial.

Purpose of the Study:

To elucidate the cellular mechanisms underlying COVID-19 severity in individuals with type I IFN deficiencies.
To analyze SARS-CoV-2 replication and cytokine production in cardiomyocytes and macrophages derived from IFNAR1 competent and deficient iPSCs.

Main Methods:

Differentiated cardiomyocytes and macrophages from IFNAR1 competent (IFNAR1^comp) and deficient (IFNAR1^def) induced pluripotent stem cells (iPSCs).
Exposed differentiated cells to SARS-CoV-2 to analyze virus replication and cytokine production.
Assessed the impact of exogenous IFNα treatment on infected cells.

Main Results:

Cardiomyocytes expressed ACE2 and supported high SARS-CoV-2 replication, which was exacerbated in IFNAR1^def cells.
Exogenous IFNα mitigated infection in IFNAR1^comp cardiomyocytes but not in IFNAR1^def cells.
Macrophages did not support SARS-CoV-2 replication but produced pro-inflammatory cytokines; this response was impaired in IFNAR1^def macrophages.

Conclusions:

Type I IFNs play a dual role: they decrease SARS-CoV-2 replication in human iPSC-derived cardiomyocytes.
Type I IFNs enhance cytokine responses in macrophages, contributing to inflammation.