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Selenium and host defence towards viruses

Published online by Cambridge University Press:  28 February 2007

Melinda A. Beck
Melinda A. Beck*
Affiliation:
Pediatrics and Nutrition, 535 Burnett-Womack Building, CB# 7220, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599–7220, USA
*
Corresponding Author: Dr Melinda A. Beck, fax +1 919 966 0135, email melinda_beck@unc.edu
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Abstract

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The association between viral disease and nutrition has long been thought to be due to effects on the host immune system. This theory suggests that when a host is malnourished, the immune system is compromised, and thus increased susceptibility to viral infection will occur. However, the virus itself may also be affected by the nutritional status of the host. We have demonstrated that a normally-benign strain of coxsackievirus B3 (CVB3/0) becomes virulent in either Se-deficient or vitamin E-deficient mice. Although the deficient animals are immunosuppressed, the virus itself is also altered. Six nucleotide changes were found in the virus that replicated in the deficient mice, and once these mutations occurred, even mice with normal nutrition became susceptible to disease. Thus, the nutritional status of the host was able to transform an avirulent virus into a virulent one due to genomic changes in the virus. We believe that a common mechanism of oxidative stress is the underlying cause of the genetic changes. Both vitamin E and Se act as antioxidants, and benign virus inoculated into GSH peroxidase (EC 1.11.1.9)-knockout mice will also convert to virulence due to genomic changes. Our work points to the importance of host nutrition during a viral disease, not only from the perspective of the host, but from the perspective of the viral pathogen as well.

Keywords

CoxsackievirusNutritional deficiencyOxidative stressSeleniumViral mutation
Type
Symposium on ’Nutrition, infection and immunity‘
Information
Proceedings of the Nutrition Society , Volume 58 , Issue 3 , August 1999 , pp. 707 - 711
Copyright
Copyright © The Nutrition Society 1999

References

Bai, J, Wu, S, Ge, K, Deng, X & Su, C (1980) The combined effect of selenium deficiency and viral infection on the myocardium of mice. Acta Academy Medical Sinica 2, 31–33.Google ScholarPubMed
Beck, MA, Esworthy, RS, Ho, Y-S & Chu, F-F (1998) Glutathione peroxidase protects mice from viral-induced myocarditis. FASEB Journal 12, 1143–1149.CrossRefGoogle ScholarPubMed
Beck, MA, Kolbeck, PC, Rohr, LH, Shi, Q, Morris, VC, Mas, P, Pelegrino, JL, Guzman, MG, Comellas, MM, Resìk, S, Alva Rodrìguez, R, Mune, M, Capo, V, Balmaseda, A, Rodrìguez, L, Rodrìguez Handy, J, Kouri, G & Llop, A (1994 a) Benign human enterovirus becomes virulent in selenium-deficient mice. Journal of Medical Virology 43, 166–170.CrossRefGoogle ScholarPubMed
Beck, MA, Kolbeck, PC, Rohr, LH, Shi, Q, Morris, VC, Mas, P, Pelegrino, JL, Guzman, MG, Comellas, MM, Resìk, S, Alva Rodrìguez, R, Mune, M, Capo, V, Balmaseda, A, Rodrìguez, L, Rodrìguez Handy, J, Kouri, G & Llop, A (1994 b) Vitamin E deficiency intensifies the myocardial injury of coxsackievirus B3 infection in mice. Journal of Nutrition 124, 345–358.CrossRefGoogle Scholar
Beck, MA, Kolbeck, PC, Shi, Q, Rohr, LH, Morris, VC, Mas, P, Pelegrino, JL, Guzman, MG, Comellas, MM, Resìk, S, Alva Rodrìguez, R, Mune, M, Capo, V, Balmaseda, A, Rodrìguez, L, Rodrìguez Handy, J, Kouri, G & Llop, A (1994 c) Increased virulence of a human enterovirus (coxsackievirus B3) in selenium-deficient mice. Journal of Infectious Diseases 170, 351–357.CrossRefGoogle ScholarPubMed
Beck, MA & Levander, OA (1998) Dietary oxidative stress and the potentiation of viral infection. Annual Review of Nutrition 18, 93–116.CrossRefGoogle ScholarPubMed
Beck, MA, Shi, Q, Morris, VC & Levander, OA (1995) Rapid genomic evolution of a non-virulent coxsackievirus B3 in selenium-deficient mice results in selection of identical virulent isolates. Nature Medicine 1, 433–436.CrossRefGoogle ScholarPubMed
Chen, C, Zhou, J, Zu, H, Jiang, Y & Zhu, G (1997) Effect of selenium supplementation on mice infected with LP-BM5 MuLY, a murine AIDS model. Biological Trace Element Research 59, 187–193.CrossRefGoogle Scholar
Cuba Neuropathy Field Investigation Team (1995) Epidemic optic neuropathy in Cuba - Clinical characterization and risk factors. New England Journal of Medicine 333, 1176–1182.CrossRefGoogle Scholar
Domingo, E & Holland, JJ (1994) Mutation rates and rapid evolution of RNA viruses. In The Evolutionary Biology of Viruses, pp. 161–184[Morse, SS, editor]. New York: Raven Press.Google Scholar
Domingo, E, Holland, JJ, Biebricher, C & Eigen, M (1995) Quasispecies: The concept and the word. In Molecular Evolution of the Viruses, pp. 171–180 [Gibbs, A, Calisher, C and Garcia-Arenal, F, editors]. Cambridge: Cambridge University Press.Google Scholar
Ge, KY, Xue, A & Bai, J (1983) Keshan disease - an endemic cardiomyopathy in China. Virchows Archives 401, 1–14.CrossRefGoogle ScholarPubMed
Gu, BQ (1983) Pathology of Keshan disease. A comprehensive review. Chinese Medical Journal 96, 251–261.Google ScholarPubMed
Harbige, LS (1996) Nutrition and immunity with emphasis on infection and autoimmune disease. Nutrition and Health 10, 285–312.CrossRefGoogle ScholarPubMed
Keshan Disease Research Group of the Chinese Academy of Medical Sciences (1979) Observations on effect of sodium selenite in prevention of Keshan disease. Chinese Medical Journal 92, 471–476.Google Scholar
Kukreja, R & Khan, A (1998) Effect of Se deficiency and its supplementation on DTH response, antibody forming cells and antibody titre. Indian Journal of Experimental Biology 36, 203–205.Google Scholar
Li, Y, Wang, F, Kang, D & Li, C (1985) Keshan disease: an endemic cardiomyopathy in China. Human Pathology 16, 602–609.CrossRefGoogle ScholarPubMed
Li, Y, Yang, Y & Chen, H (1995) Detection of the enteroviral RNA in paraffin-embedded myocardial tissue from patients with Keshan disease by nested PCR. Chung Hua I Hsueh Tsa 75, 344–345.Google ScholarPubMed
Mas, P, Pelegrino, JL, Guzman, MG, Comellas, MM, Resik, S (1997) Viral isolation from cases of epidemic neuropathy in Cuba. Archives of Pathology and Laboratory Medicine 121, 825–833.Google ScholarPubMed
Scrimshaw, N (1975) Nutrition and infection. Progress in Food Nutrition Science 1, 393–420.Google ScholarPubMed
Scrimshaw, NS, Taylor, CE, & Gordon, JE (1968) Interactions of Nutrition and Infection. WHO Monograph Series no. 57, Geneva: WHO.Google Scholar
Steinhauer, D, Domingo, E & Holland, JJ (1992) Lack of evidence for proofreading mechanisms associated with an RNA virus polymerase. Gene 122, 281–288.CrossRefGoogle ScholarPubMed
Su, C, Gong, C, Li, J, Chen, L, Zhou, D & Jin, Q (1979) Preliminary results of viral etiology of Keshan disease. Chinese Medical Journal 59, 466–472.Google Scholar