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Updated: May 10, 2026
08:11
Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
Published on: November 11, 2022
Coxsackievirus B3 modulates cardiac ion channels
Katja Steinke1, Frank Sachse, Nicole Ettischer
12Institut für Genetik von Herzerkrankungen (IfGH), Abteilung Myozelluläre Elektrophysiologie, Albert-Schweitzer-Campus 1 (Gebäude D3), D-48149 Münster. guiscard.seebohm@ukmuenster.de.
Summary
Coxsackievirus B infections cause myocarditis and arrhythmias by altering cardiac ion channels. A specific genetic variant protects against these virus-induced effects, offering new therapeutic targets for heart rhythm disorders.
Area of Science:
- Cardiology
- Virology
- Molecular Biology
- Genetics
Background:
- Coxsackievirus B infections (CVBs) are a leading cause of myocarditis, often leading to life-threatening arrhythmias and sudden cardiac death.
- The precise mechanisms linking viral infection to cardiac electrical dysfunction and arrhythmias remain poorly understood.
- Virus-induced arrhythmias share similarities with conditions caused by impaired cardiac ion channel function.
Purpose of the Study:
- To investigate the effects of Coxsackievirus B3 (CVB3) on key cardiac ion channels (KCNQ1, hERG1, Cav1.2).
- To explore the impact of CVB3 infection on ion channel protein expression and localization in cardiac cells.
- To elucidate the role of genetic variations in protecting against virus-induced cardiac electrical disturbances.
Main Methods:
- Heterologous expression of cardiac ion channels (KCNQ1, hERG1, Cav1.2) to study CVB3 effects.
- Analysis of channel protein abundance and subcellular distribution in CVB3-infected murine hearts.
- In silico modeling of infected human myocytes to assess electrical and calcium signaling alterations.
- Evaluation of the antiviral compound AG7088 and the KCNQ1 P448R polymorphism.
Main Results:
- CVB3 infection modulated the time-dependent properties of KCNQ1, hERG1, and Cav1.2 channels.
- Infected murine hearts showed altered channel protein abundance and subcellular localization.
- In silico analyses revealed significant disruptions in electrical and calcium signaling, increasing arrhythmogenesis risk.
- The KCNQ1 P448R polymorphism attenuated virus-induced channel modifications and arrhythmogenesis.
Conclusions:
- CVB3 infection directly impacts cardiac ion channel function and localization, providing a novel explanation for enteroviral myocarditis-associated arrhythmias.
- The antiviral compound AG7088 did not prevent these virus-induced channel alterations.
- The KCNQ1 P448R genetic variant confers protection against coxsackievirus-induced cardiac effects, highlighting its therapeutic potential.
- Findings pave the way for developing targeted therapies for arrhythmias in enteroviral myocarditis.
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