Dilated cardiomyopathy is so called when an etiological investigation is negative and no cause can be found for ventricular dilatation-hypokinesia. Current research points to genetic, immunological and infectious factors, often associated, and the passage of subclinical viral myocarditis to chronic disease. There is a lot of evidence in favour of this hypothesis. In the experimental model, the relationship between viral myocarditis and dilated cardiomyopathy has been demonstrated with, as cofactors, a genetic predisposition and an immunitary deficiency leading to an auto-immune subacute myocarditis. In the clinical setting, the enterovirus with a high cardiac tropism seems to play an epidemiological role in the genesis of dilated cardiomyopathy. The concentrations of neutralising anti-coxsackie B virus antibodies is higher in subjects with dilated cardiomyopathy than in a control population. The frequency of lymphocytic infiltration, a marker of dysimmunitary myocarditis, is variable from study to study but the presence of sequences of enterovirus genome in the myocardium could explain slow replication of the virus progressively destroying the myocytes. Techniques of molecular hybridization with or without prior genic amplification by the "Polymerase Chain Reaction" have demonstrated such sequences of specific enterovirus genome but discordant results require further studies.