G. Hufnagel et al., A NON-CARDIOVIRULENT STRAIN OF COXSACKIEVIRUS B3 CAUSES MYOCARDITIS IN MICE WITH SEVERE COMBINED IMMUNODEFICIENCY SYNDROME, European heart journal, 16, 1995, pp. 18-19
The most extensively studied animal model of coxsackievirus B3 (CVB3)-
induced inflammatory heart muscle disease is the murine model. In the
acute and chronic phase of the disease, it has been suggested that aut
oimmune mechanisms play a major role in the pathogenesis of the diseas
e. In this study, C3H mice without functional T- and B-lymphocytes (C3
H SCID) were inoculated either with a cardiovirulent (CVB3/20) or a no
n-cardiovirulent (CVB3/0) strain of coxsackievirus B3. Both viruses ca
used myocarditis in SCID mice. Furthermore, it could be demonstrated,
that CVB3/0 had mutated to a cardiovirulent phenotype, able to cause m
yocarditis in immunocompetent mice.