Myocarditis represents a heterogeneous final common pathway for myocardial inflammation of diverse etiologies and accounts for up to one-third of cases of dilated cardiomyopathy. The pathophysiology of viral myocarditis can be disaggregated into the effects of direct viral mediated injury, triggered acute and chronic autoimmune responses, and subsequent adverse remodeling. Recent research highlights the pathogenic role of persistent viral genome expression, Fas-ligand, tumor necrosis factor-α receptor 1, and antimyosin autoantibodies in the evolution of chronic systolic and diastolic heart failure. Recent refinements in endomyocardial biopsy evaluation, cardiac magnetic resonance imaging, and cytokine assays augment existing diagnostic modalities. Novel specific immunosuppressive targets aimed at interrupting myocyte injury and apoptosis, including interferon-β seem promising to date in small clinical studies performed on selected patients.