A transfection-reactivated Coxsackievirus B3 (rCVB3), from a full-length cDNA 
clone of Nancy strain, has previously been shown to be as cardiovirulent as the 
wild-type virus. Myocarditis induced by this genetically defined virus was 
compared in SWR mice with the traditional Balb/c model. SWR mice inoculated with 
rCVB3 developed more severe myocarditis but less severe pancreatitis than Balb/c 
mice. In contrast to the poor general health and frequent mortality of Balb/c 
mice following CVB3 infection, the body weight of SWR mice was not affected by 
CVB3 inoculation and no mortality occurred at titres of 10(2)-10(7) plaque 
forming units (PFU). Typical myocarditis developed in SWR mice 7 days post 
infection. Myocarditic foci consisting of necrotic myocardial fibres and 
mononuclear cell infiltrates resolved by day 30, similar to that observed in 
Balb/c. However, SWR mice were more sensitive to rCVB3-induced myocarditis than 
were Balb/c mice: mild myocarditis was induced (4/4) by as low as 10(2) PFU of 
the virus (ID50 < 10(1.5) PFU), and more severe myocarditis was seen at higher 
PFU of virus in a dose-dependent manner. The SWR model was tested with 
attenuated variants derived from cardiovirulent rCVB3. The ID50 for myocarditis 
was 10(7) PFU for a large plaque-size attenuant and 10(6) PFU for a minute 
plaque-size attenuant, indicating loss of cardiovirulence by a factor of more 
than 10(4)-10(5). rCVB3-induced SWR mouse is a sensitive and reliable model for 
myocarditis. It is useful in assessing the cardiovirulence of different CVB3 
variants and evaluating the efficacies of anti-viral therapies. It will allow 
follow-up study after high dose infection with cardiovirulent rCVB3.