Kandolf R, Canu A, Hofschneider P H
J Mol Cell Cardiol. 1985 Feb;17(2):167-81. doi: 10.1016/s0022-2828(85)80019-5.
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.
柯萨奇B病毒（1至5型）是急性病毒性心肌炎最常见的报告病因。为了在细胞水平研究该疾病的发病机制，我们通过用柯萨奇B3（CB3）病毒感染培养的人胎儿心脏细胞来模拟感染情况。这种病毒的成功复制可通过培养的胎儿心肌细胞内存在病毒颗粒以及每毫升培养基中10（8）个空斑形成单位（PFU）的高滴度子代病毒来证明。在感染后9小时内，心肌细胞网络失去自发收缩能力，随后解体并被存活感染的过度生长的成纤维细胞取代。这些细胞在几个月内持续产生CB3病毒，表明人心肌成纤维细胞存在携带状态感染。发现人成纤维细胞干扰素（IFN-β）是这种病毒复制的有效抑制剂。当人心脏细胞在以每细胞50 PFU的高输入复数用CB3病毒攻击前20小时与IFN-β孵育时，病毒产量可从1.2×1.8×10（5）PFU/ml培养基降低，证明了IFN-β在CB3病毒感染中的主要保护作用。因此，IFN-β似乎可能成为治疗柯萨奇心肌炎的有用抗病毒药物。
