Coxsackie B3 virus can replicate in cultured human foetal heart cells and is inhibited by interferon.
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.
D002478:Cells, Cultured; D004770:Enterovirus / Q000187:drug effects / Q000502:physiology*; D005260:Female; D005347:Fibroblasts / Q000382:microbiology; D006321:Heart / Q000196:embryology / Q000382:microbiology*; D006462:Hemolytic Plaque Technique; D006801:Humans; D007370:Interferon Type I / Q000494:pharmacology*; D008854:Microscopy, Electron; D011247:Pregnancy; D014779:Virus Replication / Q000187:drug effects
D007370:Interferon Type I