Desmin mutations in cardiomyocytes increase susceptibility to coxsackievirus B3 infection by impairing antiviral IFN-β response and upregulating viral receptors expression
Summary
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. © 2026. The Author(s).
| Authors | Callon D, Hovhannisyan Y, Friob G, Vartanian-Grimaldi JS, Guennec BE, Lebreil AL, Li Z, Suspène R, Andreoletti L, Fornès P, Berri F, Vartanian JP, Joanne P, Agbulut O |
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| Journal | Stem cell research & therapy |
| Publication Date | 2026 Feb 27;17(1) |
| PubMed | 41761335 |
| PubMed Central | PMC13049878 |
| DOI | 10.1186/s13287-025-04878-2 |