BENIGN HUMAN ENTEROVIRUS BECOMES VIRULENT IN SELENIUM-DEFICIENT MICE
BENIGN HUMAN ENTEROVIRUS BECOMES VIRULENT IN SELENIUM-DEFICIENT MICE
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DOI：
10.1002/jmv.1890430213
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发表时间：
1994-06-01
影响因子：
12.7
通讯作者：
LEVANDER, OA
中科院分区：
文献类型：
--
作者：
BECK, MA;KOLBECK, PC;LEVANDER, OA
柯萨奇病毒可能与硒（Se）反应性心肌病（克山病）的病因有关。在这里，我们报道了克隆和测序的心肌柯萨奇病毒B3 (CVB3/0)，在硒充足小鼠的心脏中不引起病理，在缺硒小鼠中引起广泛的心脏病理。从缺硒小鼠的心脏中恢复的CVB3/0接种到缺硒小鼠中，可引起明显的心脏损伤，表明该病毒突变为毒性基因型。我们证明了宿主营养状况在决定病毒感染严重程度中的重要作用。(C) 1994 Wiley-Liss, Inc。
Coxsackieviruses have been implicated as possible co-factors in the etiology of the selenium (Se)-responsive cardiomyopathy known as Keshan disease. Here we report that a cloned and sequenced amyocarditic coxsackievirus B3 (CVB3/0), which causes no pathology in the hearts of Se-adequate mice, induces extensive cardiac pathology in Se-deficient mice. CVB3/0 recovered from the hearts of Se-deficient mice inoculated into Se-adequate mice induced significant heart damage, suggesting mutation of the virus to a virulent genotype. We demonstrate the important role of host nutritional status in determining the severity of a viral infection. (C) 1994 Wiley-Liss, Inc.