No abstract

Previous work from our laboratory demonstrated that selenium deficiency in the mouse allows a normally benign (amyocarditic) cloned and sequenced Coxackievirus 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.

Selenium (Se) deficiency has previously been shown to induce myocarditis in mice infected with a benign strain of coxsackievirus. To determine if Se deficiency would also intensify an infection with influenza virus, Se‐deficient and Se‐adequate mice were infected with a mild strain of influenza, influenza A/Bangkok/1/79 (H3N2). Infected Se‐deficient mice developed much more severe interstitial pneumonitis than did Se‐adequate mice. This increase in pathology was associated with significant alterations in mRNA levels for cytokines and chemokines involved in pro‐inflammatory responses. These results demonstrate that adequate nutrition is required for protection against viral infection and suggest that nutritional deprivation may be one of many factors that increase the susceptibility of individuals to influenza infection.