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Micronutrients and host resistance to viral infection

Published online by Cambridge University Press:  28 February 2007

Melinda A. Beck*
Affiliation:
Departments of Pediatrics and CB #7220, University of NC at Chapel Hill, Chapel Hill, NC 27599–7220, USA Nutrition, CB #7220, University of NC at Chapel Hill, Chapel Hill, NC 27599–7220, USA
Colette C. Matthews
Affiliation:
Nutrition, CB #7220, University of NC at Chapel Hill, Chapel Hill, NC 27599–7220, USA
*
*Corresponding author: Professor Melinda Beck, fax +1 919 966 0135, email melinda_beck@unc.edu
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Abstract

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Previous work in our laboratory demonstrated that a virus could undergo rapid mutation in a host deficient in Se, leading to a normally avirulent virus acquiring virulence due to genome changes. Once these mutations occur, even a host with adequate Se-nutriture is susceptible to the newly virulent virus. What influence does the deficiency in Se have on the immune response of the host? Infection with myocarditic strains of coxsackievirus induces an inflammatory response in the cardiac tissue. It is this immune response that induces the heart damage, rather than direct viral effects on the heart tissue. Chemokines are chemo-attractant molecules that are secreted during an infection in order to attract immune cells to the site of the injury, and have been found to be important for the development of coxsackievirus-induced myocarditis. We found that a deficiency in Se influences the expression of mRNA for the chemokine monocyte chemo-attractant protein-1, which may have implications for the development of myocarditis in the Se-deficient host. Expression of mRNA for interferon-γ was also greatly decreased in the Se-deficient animal. Thus, a deficiency in Se can have profound effects on the host as well as on the virus itself. How the alteration of the immune response of the Se-deficient animal affects the development of the virulent genotype remains to be answered.

Type
Meeting Report
Copyright
Copyright © The Nutrition Society 2000

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