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Benign human enterovirus becomes virulent in selenium‐deficient mice
Author(s) -
Beck Melinda A.,
Kolbeck Peter C.,
Rohr Lisa H.,
Shi Qing,
Morris Virginia C.,
Levander Orville A.
Publication year - 1994
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.1890430213
Subject(s) - coxsackievirus , virulence , myocarditis , virology , enterovirus , virus , genotype , biology , cardiomyopathy , selenium , mutation , selenium deficiency , etiology , immunology , medicine , pathology , heart failure , gene , genetics , oxidative stress , endocrinology , chemistry , catalase , organic chemistry , glutathione peroxidase
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. © 1994 Wiley‐Liss, Inc.