Increased Virulence of a Human Enterovirus (Coxsackievirus B3) in SeleniumDeficient Mice

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Abstract
Coxsackievirus B3 (CVB3/20)-induced myocarditic lesions occurred more quickly and were more severeandvirustiters inheart and liverwerehigherinselenium(Se)-deficientthan Se-adequate mice. NK cell activity and serum neutralizing antibody titers were similar in both Se-adequate and-deficientCVB3/20-infected mice;however,lymphocyteproliferationtoboth mitogen andantigenwasdecreasedinSe-deficientmice.CVB3/20isolatedfromSe-deficientdonor mice and inoculated into Se-adequate recipient mice induced severe myocarditis. In contrast, CVB3/ 20 isolated from Se-adequate donor mice and inoculated into Se-adequate recipient mice induced only moderate myocarditis, similar to that caused by the original virus stock. Thus, the general population ofCVB3/20virions,asaconsequenceofreplicatinginanSe-deficienthost,underwent a phenotypic change to increased virulence. These results have important implications for the emergence of virulent viruses.

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