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The mechanisms underlying the development of virus\u2010induced, life\u2010threatening arrhythmias, which are pheno\u2010typically similar to those observed in patients having functionally impaired cardiac ion channels, remain, however, enigmatic. In the present study, we show, for the first time, modulating time\u2010dependent effects of CVB3 on the cardiac ion channels KCNQ1, hERG1, and Ca\n                    <jats:sub>v<\/jats:sub>\n                    1.2 in heterologous expression. Channel protein abundance in cellular plasma membrane and patterns of their subcellular distribution were altered in infected murine hearts. The antiviral compound AG7088 did not prevent these effects on channels.\n                    <jats:italic>In silico<\/jats:italic>\n                    analyses of infected human myocytes suggest pronounced alterations of electrical and calcium signaling and increased risk of arrhythmogenesis. These modifications are attenuated by the common Asian polymorphism KCNQ1 P448R, a genetic determinant preventing coxsackievirus\u2010induced effects\n                    <jats:italic>in vitro<\/jats:italic>\n                    . This study provides a previously unknown explanation for the development of arrhythmias in enteroviral myocarditis, which will help to develop therapeutic strategies for arrhythmia treatment.\u2014Steinke, K., Sachse, F., Ettischer, N., Strutz\u2010Seebohm, N., Henrion, U., Rohrbeck, M., Klosowski, R., Wolters, D., Brunner, S., Franz, W.\u2010M., Pott, L., Munoz, C., Kandolf, R., SchulzeBahr, E., Lang, F., Klingel, K., Seebohm, G., Coxsackievirus B3 modulates cardiac ion channels. 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