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ARS Home » Northeast Area » Beltsville, Maryland (BHNRC) » Beltsville Human Nutrition Research Center » Diet, Genomics and Immunology Laboratory » Research » Publications at this Location » Publication #143024

Title: COXSACKIEVIRUS B3-RESISTANT MICE BECOME SUSCEPTIBLE IN SE/VITAMIN E DEFICIENCY

Author
item BECK, MELINDA
item TOONE-WILLIAMS, DEITRA
item Levander, Orville

Submitted to: Free Radical Biology and Medicine
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/14/2003
Publication Date: 5/15/2003
Citation: Beck, M., Toone-Williams, D., Levander, O.A. 2003. Coxsackievirus b3-resistant mice become susceptible in se/vitamin e deficiency. Free Radical Biology and Medicine.

Interpretive Summary: The United States is currently experiencing an emerging epidemic of congestive heart failure (CHF). About 5 million Americans suffer from this chronic condition in which the heart loses its ability to pump blood efficiently. Among the possible causes of CHF are certain viruses that can damage heart muscle. Here we show in a mouse model that simultaneous deficiencies in two nutritional antioxidants, selenium and vitamin E, render mice normally resistant to such a virus susceptible to the virus. Dietary factors should be investigated further for their potential role in HF. If the principle demonstrated in this paper that improved nutrition can enhance the innate ability of an organism to resist infection with a disease-producing pathogen is found to be generally applicable to a variety of host/microbe interactions, these findings could launch a new awareness regarding the possibility of using dietary intervention to protect against infectious disease. This would be of benefit not only directly to mankind as a whole but would also provide indirect benefits by affording protection to the animals and perhaps plants which form the basis of man's food supply.

Technical Abstract: The severity of the heart damage caused by a coxsackievirus infection in mice is determined by several factors including the genotype of the infecting virus as well as the genetic background of the infected host. Earlier work by us showed that the cardiovirulence of a given coxsackievirus genotype could be increased substantially by feeding the host a diet nutritionally deficient in either selenium or vitamin E. Here we report that host genetic background as a determinant of viral infection outcome is superseded by feeding the host a diet nutritionally deficient in both selenium and vitamin E. Mice of the C57Bl/6 strain, normally resistant to coxsackievirus B3-induced myocarditis, become susceptible when fed such a doubly deficient diet. Our results demonstrate the powerful influence of host nutritional status on the course of viral infection compared to other variables traditionally considered to play major roles in determining the extent of virally-induced inflammatory heart disease.