Nature Medicine
1, 433 - 436 (1995)
doi:10.1038/nm0595-433
Rapid genomic evolution of a non-virulent Coxsackievirus B3 in selenium-deficient mice results in selection of identical virulent isolatesMelinda A. Beck1, 3, Qing Shi1, Virginia C. Morris2
& Orville A. Levander2
1Frank Porter Graham Child Development Center, CB #8180, University of North Carolina at Chapel Hill, 105 Smith Level Road, Chapel Hill, NC 27599-8180, USA
2Nutrient Requirements and Functions Laboratory, United States Department of Agriculture, Agricultural Research Service, Beltsville Human Nutrition Research Center, Building 307, Room 220, Beltsville, MD 20705, USA
3Correspondence should be addressed to M.A.B. Previous work from our laboratory demonstrated that selenium deficiency in the mouse allows a normally benign (amyocarditic) cloned and sequenced Coxsackievirus to cause significant heart damage. Furthermore, Coxsackievirus recovered from the hearts of selenium-deficient mice inoculated into selenium-adequate mice still induced significant heart damage, suggesting that the amyocarditic Coxsackievirus had mutated to a virulent phenotype. Here we report that sequence analysis revealed six nucleotide changes between the virulent virus recovered from the selenium-deficient host and the avirulent input virus. These nucleotide changes are consistent with known differences in base composition between virulent and avirulent strains of Coxsackievirus. To the best of our knowledge, this is the first report of a specific nutritional deficiency driving changes in a viral genome, permitting an avirulent virus to acquire virulence due to genetic mutation.
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