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Rapid genomic evolution of a non-virulent coxsackievirus B3 in selenium-deficient mice

M A Beck1

  • 1University of North Carolina at Chapel Hill, Frank Porter Graham Child Development Center 27599-8180, USA.

Biomedical and Environmental Sciences : BES
|October 7, 1997
PubMed

Insights

Keshan disease prevention involves selenium (Se) supplementation. Selenium deficiency exacerbates coxsackievirus B3 (CVB3) myocarditis, increasing viral virulence and causing mutations.

Area of Science:

  • Cardiology
  • Virology
  • Nutritional Science

Background:

  • Keshan disease, an endemic cardiomyopathy in China, is linked to selenium (Se) deficiency.
  • The disease's seasonal and annual patterns suggest an infectious co-factor is involved alongside Se deficiency.

Purpose of the Study:

  • To investigate the role of selenium (Se) deficiency in coxsackievirus B3 (CVB3)-induced myocarditis.
  • To determine if Se deficiency influences CVB3 virulence and genetic mutations.

Main Methods:

  • A murine model of coxsackievirus B3 (CVB3)-induced myocarditis was utilized.
  • Selenium-deficient mice were compared to control groups for susceptibility to CVB3 and viral changes.

Main Results:

  • Se-deficient mice exhibited increased susceptibility to the cardiopathologic effects of CVB3.
  • A normally benign CVB3 strain became virulent in Se-deficient mice, indicating a change in pathogenicity.
  • Viral genome analysis revealed point mutations in CVB3 isolated from Se-deficient mice.

Conclusions:

  • Selenium deficiency plays a critical role in the development and severity of CVB3-induced myocarditis.
  • Se deficiency can induce mutations in CVB3, potentially increasing its virulence.
  • Oxidative stress in Se-deficient hosts may contribute to viral mutation and altered host immune responses.

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