The six serotypes of the group B coxsackieviruses (CVB) are common human en
teroviruses linked etiologically to inflammatory cardiomyopathies. This has
been demonstrated by molecular detection of enteroviral RNA in human heart
tissue, serologic associations with disease, and virus isolation from case
s of fulminant myocarditis. The murine model of CVB-associated myocarditis
has demonstrated that CVB can be attenuated through mutations at different
genomic sites. Human CVB3 isolates demonstrate varying degrees of cardiovir
ulence in the murine model; one site of virulence determination has been ma
pped to domain II of the 5' non-translated region. The interplay of CVB rep
lication and the immune response to that replication in the heart is a comp
lex interaction determining the extent to which the virus replication is li
mited and the degree to which a pathogenic inflammation of cardiac muscle o
ccurs, Studies of CVB3-induced myocarditis in murine strains lacking subset
s of the immune system or genes regulating the immune response have demonst
rated a pivotal role of the T cell response to the generation of myocarditi
s. While CVB are associated with 20-25% of cases of myocarditis or cardiomy
opathy, the severity of the disease and the existence of attenuated strains
shown to generate protective immunity in animal models indicates that vacc
ination against the CVBs would be valuable. Copyright (C) 2001 John Wiley &
Sons, Ltd.