Coxsackie B viruses (types 1 to 5) are the most frequent reported cause of acute 
viral myocarditis. To study the pathogenesis of the disease at the cellular 
level, we simulated an infectious situation by infecting cultured human foetal 
heart cells with Coxsackie B3 (CB3) virus. Successful replication of this virus 
could be demonstrated by the presence of virus particles inside cultivated 
foetal myocytes together with high titres of progeny virus of 10(8) 
plaque-forming units (PFU) per millilitre culture medium. Within 9 h of 
infection networks of myocytes lost their ability to contract spontaneously 
followed by disintegration and replacement by overgrowing fibroblasts which 
survived the infection. These cells produced CB3 virus continuously over several 
months, indicating carrier state infection of human myocardial fibroblasts. 
Human fibroblasts interferon (IFN-beta) was found to act as a potent inhibitor 
of the replication of this virus. Virus yields could be reduced from 1.2 x 1.8 x 
10(5) PFU/ml culture medium when human heart cells were incubated with IFN-beta 
20 h prior to challenge with a high input multiplicity of 50 PFU of CB3 virus 
per cell, demonstrating the major protective role of IFN-beta in CB3 viral 
infection. It thus appear that IFN-beta might become useful as an antiviral 
agent in the treatment of Coxsackie myocarditis.