Desmin mutations in cardiomyocytes increase susceptibility to coxsackievirus B3 infection by impairing antiviral IFN-β response and upregulating viral receptors expression

CVB3/28 infection compromises the structural integrity and contractile function of cardiomyocytes and exerts a more severe effect in cells harboring DES mutations. These findings underscore a pathogenic synergy between genetic cytoskeletal defects and viral infection, revealing a mechanistic basis for the heightened vulnerability of patients carrying mutation in DES gene to virus-induced cardiac decompensation. CVB3/28 infection disrupts cardiomyocyte structure and impairs contractility, with more severe effects in cells carrying DES mutations. By enhancing viral replication and weakening antiviral defenses, DES mutations act synergistically with CVB3/28 infection to increase the risk of cardiac dysfunction.

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Publication Details

Journal
Stem Cell Research & Therapy
Published
2026-02-27
DOI
https://doi.org/10.1186/s13287-025-04878-2
Primary Topic
Viral Infections and Immunology Research
Type
article
Field-Weighted Citation Impact
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article

Desmin mutations in cardiomyocytes increase susceptibility to coxsackievirus B3 infection by impairing antiviral IFN-β response and upregulating viral receptors expression

Rodolphe Suspène, Jean‐Pierre Vartanian, Yeranuhi Hovhannisyan, Fatma Berri et al.
Stem Cell Research & Therapy
Viral Infections and Immunology Research
article

Desmin mutations in cardiomyocytes increase susceptibility to coxsackievirus B3 infection by impairing antiviral IFN-β response and upregulating viral receptors expression

Rodolphe Suspène, Jean‐Pierre Vartanian, Yeranuhi Hovhannisyan, Fatma Berri, Pierre Joanne, Zhenlin Li, Jean-Sébastien Vartanian-Grimaldi, Domitille Callon, Gabriel Friob, Paul Fornés, Brice-Emmanuel Guennec, Anne-Laure Lebreil, Onnik Agbulut, Laurent Andreoletti
article en

Abstract

CVB3/28 infection compromises the structural integrity and contractile function of cardiomyocytes and exerts a more severe effect in cells harboring DES mutations. These findings underscore a pathogenic synergy between genetic cytoskeletal defects and viral infection, revealing a mechanistic basis for the heightened vulnerability of patients carrying mutation in DES gene to virus-induced cardiac decompensation. CVB3/28 infection disrupts cardiomyocyte structure and impairs contractility, with more severe effects in cells carrying DES mutations. By enhancing viral replication and weakening antiviral defenses, DES mutations act synergistically with CVB3/28 infection to increase the risk of cardiac dysfunction.

Stem Cell Research & Therapy
Centre National de la Recherche Scientifique (FR), Inserm (FR), Institut Pasteur (FR), Université Paris Cité (FR), Sorbonne Université (FR), Centre Hospitalier Universitaire de Reims (FR), Institut de Biologie Paris-Seine (FR), Department of Virology (FR), Développement Adaptation et Vieillissement (FR), Université de Reims Champagne-Ardenne (FR)
Openalex Percentile: Top 46%
Viral Infections and Immunology Research
DOIOpen Access PDFOpenAlex
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