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良性人类肠道病毒在缺硒小鼠中变得具有毒性。

Benign human enterovirus becomes virulent in selenium-deficient mice.

作者信息

Beck M A, Kolbeck P C, Rohr L H, Shi Q, Morris V C, Levander O A

机构信息

Frank Porter Graham Child Development Center, University of North Carolina, Chapel Hill.

出版信息

J Med Virol. 1994 Jun;43(2):166-70. doi: 10.1002/jmv.1890430213.

Abstract

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.

摘要

柯萨奇病毒被认为可能是克山病(一种对硒有反应的心肌病)病因中的辅助因素。在此我们报告,一种克隆并测序的无心肌炎柯萨奇病毒B3(CVB3/0),在硒充足的小鼠心脏中不会引起病变,但在缺硒小鼠中会诱发广泛的心脏病变。从接种到硒充足小鼠体内的缺硒小鼠心脏中分离出的CVB3/0会导致显著的心脏损伤,这表明病毒已突变为致病基因型。我们证明了宿主营养状况在决定病毒感染严重程度方面的重要作用。

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