The human enteroviruses, especially the coxsackie B viruses, have been
established as aetiologic agents of human inflammatory heart disease,
a condition which may lend to dilated cardiomyopathy and heart failur
e. It is clear from murine models of coxsackievirus B3-induced inflamm
atory heart disease that not all strains of the virus are cardiovirule
nt (able to cause disease). Here, we present preliminary data mapping
the sire in a coxsackievirus B3 genome which determines a cardiovirule
nt phenotype.