Benign human enterovirus becomes virulent in selenium-deficient mice

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


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Coxsackievirus Infections / microbiology*
  • Enterovirus B, Human / pathogenicity*
  • Male
  • Mice
  • Mice, Inbred C3H
  • Myocarditis / microbiology*
  • Selenium / deficiency*
  • Virulence / genetics


  • Selenium