INCREASED VIRULENCE OF A HUMAN ENTEROVIRUS (COXSACKIEVIRUS B3) IN SELENIUM-DEFICIENT MICE

Coxsackievirus B3 (CVB3/20)-induced myocarditic lesions occurred more quickly and were more severe and virus titers in heart and liver were higher in selenium (Se)-deficient than Se-adequate mice. NK cell activ ity and serum neutralizing antibody titers were similar in both Se-ade quate and -deficient CVB3/20-infected mice; however, lymphocyte prolif eration to both mitogen and antigen was decreased in Se-deficient mice . CVB3/20 isolated from Se-deficient donor 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-adequa te recipient mice induced only moderate myocarditis, similar to that c aused by the original virus stock. Thus, the general population of CVB 3/20 virions, as a consequence of replicating in an Se-deficient host, underwent a phenotypic change to increased virulence. These results h ave important implications for the emergence of virulent viruses.