The VP1-unique region of parvovirus B19 induces myocardial injury in mice
The VP1-unique region of parvovirus B19 induces myocardial injury in mice
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细小病毒 B19 的 VP1 独特区域诱导小鼠心肌损伤
DOI：
10.3109/00365540903321580
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发表时间：
2010-01-01
影响因子：
--
通讯作者：
Li, Yunming
中科院分区：
文献类型：
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作者：
Nie, Xiaojing;Zhang, Guocheng;Li, Yunming
细小病毒B19（B19 V）作为一种常见的人类病原体，已被证明与心肌炎、心肌病和心包炎等许多心脏病有关。病毒蛋白1独特区（VP 1u）是B19病毒感染的关键，但其在B19病毒诱导的心肌损伤的发病机制中的作用尚未得到很好的研究。为了研究VP 1u对宿主心肌的影响，我们首先在大肠杆菌中表达了重组VP 1u蛋白，通过高容量发酵进行了大规模生产，并使用AKTA explorer 100系统对其进行了纯化。用重组蛋白治疗小鼠后，我们检查了心肌形态学的变化、抗VP 1u蛋白抗体的滴度和一组心脏功能蛋白标志物。我们的研究结果表明，VP 1u单独足以引起宿主心肌的病理和超微结构变化，并增加功能酶天冬氨酸转氨酶（AST），乳酸脱氢酶（LDH），肌酸激酶（CK），肌酸激酶同工酶（CK-MB）和α-羟丁酸脱氢酶（α-HBDH）的水平。心肌病理学和心肌酶谱的变化提示B19 V的VP 1u蛋白可引起心肌损伤，可能在B19 V所致心脏病的发病机制中起重要作用。
As a common human pathogen, parvovirus B19 (B19V) has been shown to be associated with many heart diseases, such as myocarditis, cardiomyopathy and cardiopericarditis. The virus protein 1-unique region (VP1u) is critical to B19V infectivity, but its role in the pathogenesis of B19V-induced myocardial injury has not been well studied. In this study to investigate the effects of VP1u on the host myocardium, we first expressed a recombinant VP1u protein in Escherichia coli, produced it on a large scale by high-volume fermentation, and purified it using the AKTA explorer 100 system. Following treatment of mice with the recombinant protein, we then examined changes in the morphology of the cardiac muscles, the titre of anti-VP1u protein antibodies, and a panel of heart functional protein markers. Our results show that VP1u alone is sufficient to elicit pathological and ultrastructural changes in the host myocardium, and to increase the levels of the functional enzymes aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine kinase (CK), creatine kinase isoenzyme (CK-MB) and alpha-hydroxybutyric acid dehydrogenase (alpha-HBDH). The changes in myocardial pathology and myocardial zymogram indicate that the VP1u protein of B19V causes myocardial injury, and may largely contribute to the pathogenesis of B19V-induced heart diseases.