Over the past year there have been few significant breakthroughs in the understanding of the etiologies of viral myocarditis or dilated cardiomyopathy (DCM). One interesting trend has been the increasing number of reports of myocarditis associated with parvovirus B19 infection. Whether this is simply a result of improved diagnostics, or reflects an underlying change in the etiology is unclear. However, studies of the underlying mechanisms of these disorders have resulted in several reports linking the acquired and viral forms. Over the past few years the cytoarchitecture has been a focus of study for familial DCM. During the last year, one key molecule, dystrophin, has been shown to be disrupted in patients with end-stage cardiomyopathy, irrespective or etiology, mutated in patients with sporadic forms of disease and identified as a potential susceptibility gene for viral infection of the myocardium. The shared cellular receptor, the Coxsackievirus B-Adenovirus receptor (CAR), for the two most common viral agents associated with acquired myocarditis and DCM, was shown to be up-regulated in patients with DCM, potentially making the expression of this protein a marker of susceptibility to virus infection. However, a study of the CAR gene in patients with DCM or myocarditis did not identify any genetic mutations in these patients. Finally a receptor for viral double stranded RNA (TLR-3) was identified. The role of this receptor in the innate immune response against cardiotropic viruses has yet to be elucidated.