Virus-associated heart disease results in a complex interaction between the viral genome, virus-triggered immune processes, and the heart, giving rise to a range of myocardial complaints. Many of the mechanisms leading to chest pain, arrhythmia, and heart failure are still speculative. Virus-related chest pain is often associated with direct infection of vascular endothelial cells, causing endothelial dysfunction, vasospasm, or focal ischemia. Virusinduced structural changes and consecutive changes in ventricular dynamics, vascular changes, or insufficient energy supply may trigger severe arrhythmia and heart failure. Further infected myocyte loss occurs with virus clearance. Myocardial damage and clinical symptoms depend on the cellular virus infection plus the virus- and innate immune-mediated myocardial injury...