Article Dans Une Revue Journal of Clinical Immunology Année : 2025

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

Verónica Durán
  • Fonction : Auteur
Eirini Nikolouli
  • Fonction : Auteur
Shambhabi Chatterjee
  • Fonction : Auteur
Bibiana Costa
  • Fonction : Auteur
Andreas Pavlou
  • Fonction : Auteur
Annett Ziegler
  • Fonction : Auteur
Jennifer Becker
  • Fonction : Auteur
Kira Baumann
  • Fonction : Auteur
Matthias Bruhn
  • Fonction : Auteur
Anna Rafiei Hashtchin
  • Fonction : Auteur
Yvonne Lisa Behrens
  • Fonction : Auteur

Résumé

Abstract The cellular basis of COVID-19 severity in patients with deficiencies in type I IFN immunity remains unclear. In this study, we differentiated cardiomyocytes and macrophages from IFNAR1 competent (IFNAR1 comp ) and deficient (IFNAR1 def ) induced pluripotent stem cells (iPSCs), and analyzed virus replication and cytokine production after exposure to SARS-CoV-2. Cardiomyocytes expressed the SARS-CoV-2 receptor angiotensin-converting enzyme 2 (ACE2) and showed abundant SARS-CoV-2 replication, which was higher in IFNAR1 def than IFNAR1 comp cells. Treatment with exogenous IFNα mitigated infection in IFNAR1 comp , but not in IFNAR1 def cardiomyocytes. In contrast, macrophages did not express ACE2 and did not support SARS-CoV-2 replication, but produced pro-inflammatory cytokines upon virus exposure, which was impaired in IFNAR1 def macrophages. In conclusion, type I IFNs decrease SARS-CoV-2 replication in human iPSC-derived cardiomyocytes, while they increase cytokine responses of macrophages.

Dates et versions

hal-05330521 , version 1 (24-10-2025)

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Citer

Verónica Durán, Eirini Nikolouli, Shambhabi Chatterjee, Bibiana Costa, Andreas Pavlou, et al.. Type I IFNs Decrease SARS-CoV-2 Replication in Human Cardiomyocytes and Increase Cytokine Production in Macrophages. Journal of Clinical Immunology, 2025, 45 (1), pp.149. ⟨10.1007/s10875-025-01943-6⟩. ⟨hal-05330521⟩

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