Submitted to: Journal of Free Radical Biology and Medicine
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/4/2004
Publication Date: 1/1/2005
Citation: Beck, M.A., Shi, Q., Morris, V.C., Levander, O.A. 2005. Benign coxsackie virus damages heart muscle in iron-loaded vitamin E-deficient mice. Journal of Free Radical Biology and Medicine. 38:(1)112-116. Interpretive Summary: Iron deficiency anemia is the most common nutritional deficiency in the world, affecting an estimated one Billion (not million) individuals. Hence, it is quite common to supplement people with iron to prevent and/or cure anemia. Here we report that giving too much iron to mice, however, results in viral-induced heart damage even if that virus causes no heart problems in mice given normal amounts of iron. Of concern are recent reports by others that administering nutritional levels of iron has a deleterious effect on the progression of AIDS. These results, coupled with our own, have frightening implications since giving iron pills is a routine, widespread, and generally accepted feature of public health nutrition. Clearly, more needs to be learned about the effects of iron supplements on viral virulence.
Technical Abstract: Several oxidative stressors allow a normally benign coxsackievirus B3 (CVB3/0) to exert a cardiopathologic effect in host mice. The study reported here investigated whether dietary iron overload, another oxidant stress, would also permit CVB3/0 to damage heart muscle in vitamin E-deficient (-VE) mice. Four groups of mice were fed either a 'VE or a +VE diet containing either a normal or excessive (30X) amount of iron. After 4 weeks of feeding, the mice were inoculated with CVB3/0 and heart damage was assessed at various times thereafter. The severest heart damage occurred in the group fed the -VE diet containing excess iron. However, mice fed the +VE excess iron diet developed heart damage equal to that in mice fed the -VE diet with normal iron. No damage was observed in infected mice fed the +VE diet containing normal iron. Further research is needed to clarify the role of oxidative stress and iron overload in determining the course of viral infection