SARS-CoV-2 Spike Protein-Mediated Cardiac Dysfunction: Structural Abnormalities, Impaired Calcium Dynamics, and Gene
Chen-Yu Huang1,2,3,4,5, Chia-Chi Cheng1, Si-Han Chen1
1Department of Medical Laboratory Science and Biotechnology, National Cheng Kung University, Tainan, Taiwan.
Journal of Medical Virology
|January 6, 2026
Summary
The SARS-CoV-2 spike protein directly harms heart cells, causing structural and functional damage. This study used a pseudovirus model to show the spike protein
Area of Science:
- Cardiology
- Virology
- Molecular Biology
Background:
- COVID-19, caused by SARS-CoV-2, presents significant cardiovascular complications.
- The SARS-CoV-2 spike protein may directly induce cardiac dysfunction via ACE2 receptors on cardiomyocytes.
Purpose of the Study:
- To investigate the direct impact of SARS-CoV-2 spike proteins (Wuhan and Delta variants) on cardiomyocytes.
- To establish and utilize a lentiviral pseudovirus system for modeling SARS-CoV-2 cardiac injury.
Main Methods:
- Developed a lentiviral pseudovirus system expressing Wuhan and Delta SARS-CoV-2 spike proteins.
- Exposed human embryonic stem cell-derived cardiomyocytes (ESC-CMs) to pseudoviruses.
- Analyzed structural changes (sarcomere length, syncytium formation), calcium transient dynamics, and gene expression.
Main Results:
- Pseudovirus exposure increased sarcomere length and induced syncytium formation in ESC-CMs.
- Early disturbances in intracellular calcium transients were observed post-infection.
- Transcriptomic analysis revealed dysregulation of genes involved in cardiac cell junctions, structure, and ion/calcium handling.
Conclusions:
- The lentiviral pseudovirus platform effectively models SARS-CoV-2-induced cardiac injury.
- The SARS-CoV-2 spike protein plays a direct pathogenic role in cardiac abnormalities.
- Findings highlight the spike protein's contribution to structural, functional, and molecular cardiac damage.
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