VITAMIN-E-DEFICIENCY INTENSIFIES THE MYOCARDIAL INJURY OF COXSACKIEVIRUS B3 INFECTION OF MICE

Feeding a vitamin E-deficient diet increases pathology in hearts of mi ce infected with a myocarditic coxsackievirus B3 (CVB3/20). Hearts fro m infected mice fed a vitamin E-deficient diet rich in highly unsatura ted fat (menhaden oil) exhibited more severe pathology than hearts fro m infected mice fed a vitamin E-deficient diet based largely on satura ted fat (lard). Furthermore, a cloned and sequenced amyocarditic coxsa ckievirus B3 (CVB3/0), which caused little or no pathology in the hear ts of vitamin E-supplemented mice, induced extensive cardiac pathology in vitamin E-deficient mice. In infected mice, both mitogen and antig en responses were depressed by vitamin E deficiency, although neutrali zing antibody responses were unaffected. Natural killer cell responses were comparable in infected mice fed a lard-based diet with or withou t supplemented vitamin E. However, a menhaden oil-based diet, whether supplemented with vitamin E or not, significantly depressed natural ki ller cell activity in infected mice compared with mice fed the lard-ba sed diet. Coxsackievirus B3/0 recovered from the heart of a vitamin E- deficient donor mouse, passaged one time onto HeLa cells, caused signi ficant heart damage when passed back into vitamin E-supplemented recip ient mice, demonstrating that the amyocarditic CVB3/0 had changed to a virulent phenotype. Enhanced virulence was also seen with CVB3/20 vir us similarly passaged in a vitamin E-deficient donor. Our work demonst rates the important role of host nutritional antioxidant status in det ermining the severity of certain viral infections.