Military Strategies for Sustainment of Nutrition and Immune Function in the Field (1999) / Chapter Skim
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16 Trace Minerals, Immune Function, and Viral Evolution
16 Trace Minerals, Immune Function, and Viral Evolution
Pages 337-359
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National Academy Press Trace Minerals' Immune Function' and Viral Evolution Melinda A Becky INTRODUCTION A number of trace elements have been shown to be important for adequate functioning of the immune system, including copper, zinc, and selenium.
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Excess levels of Zn have also been reported to be immunosuppressive, including decreased activities of polymorphonuclear leukocytes, decreased T-cell proliferation to mitogen, and decreased antibody production (Schlesinger et al., 1993~. Thus, Zn status, both excess and deficient, adversely affects immune function.
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Animal studies have demonstrated that Cu-deficient mice have impaired plaque formation to sheep blood red cells, demonstrating decreased B-cell activity, and decreased antibody responses to a number of antigens (Blakly and Hamilton, 1987; Failla et al., 1988; Koller, 1987; Prohaska and Lukasewycz, 1981, 1989, 1990; Vyas and Chandra, 1983~. Cell-mediated immunity has also been studied in Cu-deficient animals, with conflicting results.
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Se deficiency has been associated with lower resistance to infection with Pasturella multocida and parainfluenza 3 virus (Chandra and Chandra, 1986; Dhur et al., 1990; Larsen, 1988; Larsen and Tollersund, 1981; Reffett et al., 1988; Sheffy and Schultz, 1979, Stable and Spears, 1993~. The increased susceptibility to infectious pathogens in Se deficiency may be due to decreased antibody production and impaired lymphoproliferative responses (Chandra and Chandra, 1986~.
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is characterized by acute or chronic heart conditions affecting heart function such as cardiac insufficiency, enlargement of the heart, arrhythmia, atrial fibrillation, and tachycardia (Li et al., 1985~. Histologically, KD is characterized by multiple focal necrosis and myocardial parenchymatous degeneration (Gu, 1983~.
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Strains of mice that can clear virus from the heart more rapidly and rapidly produce neutralizing antibody develop only a mild myocarditis. However, strains of mice that have delayed viral clearance and delayed production of neutralizing antibody develop severe myocarditis (Herskovitz et al., 1985~.
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Scores: 0, no lesions; 1+, foci of mononuclear cell inflammation associated with myocardial cell reactive changes without myocardial cell necrosis; 2+, inflammatory foci clearly associated with myocardial cell reactive changes; 3+ - 4+, inflammatory foci clearly associated with myocardial cell necrosis and dystrophic calcification. Each bar represents the mean +/-SD of 10 mice.
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Thus, because either Se or vitamin E deficiency enhanced CVB3/20-induced myocarditis and allowed a normally benign CVB3/0 infection to become virulent, this author and colleagues proposed a common mechanism of oxidative stress. Viral titers in various organs were examined to determine if viral replication patterns were altered as a result of replication in a nutritionally deficient animal.
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Se and/or vitamin E deficiencies have a number of effects on immune function, including decreased proliferative responses to mitogen and reduced antibody production. For studies in this laboratory, several immune functions that are important in viral clearance mechanisms were examined: (1)
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-Se 1 ~ 0 5 10 15 Stimulation Index 20 25 CVB3/20 I I CVB3/0 FIGURE 16-6 CVB3-antigen-specific-stimulated, spleen cell proliferative responses from Se-adequate (+Se) or Se-deficient (-Se)
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Although exposure to mitogen could induce stimulation of INF-y mRNA in cells from Se-deficient mice, it is not known if antigen stimulation of cells from CVB3-infected, Se-deficient mice can also stimulate mRNA for INFIX. Thus, although neutralizing antibody and NK levels are unaffected, or slightly affected, under these conditions of nurture, proliferation levels and mRNA for IL-6 and TNF-p are depressed in Se-deficient mice, which indicates that some immune dysfunction has occurred.
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The increased pathology seen in nutritionally deficient mice may have been due to changes in the host that allowed for the virus to cause increased damage, such as a decreased immune response or changes in heart cell physiology. A second possibility is that the virus itself changed as a consequence of replication in a Se-deficient host.
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This laboratory was able to demonstrate that viruses from either Se- or vitamin E-deficient mice underwent a phenotypic change in the deficient animal, such that passage into a Se- and vitamin E-supplemented recipient also caused increased disease (Beck et al., 1994a, b, c)
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Recently, this laboratory isolated virus from CVB3/0-infected, vitamin Edeficient mice. Identical nucleotide changes occurred in these viruses as well, suggesting that a common mechanism of oxidative stress leads to predictable nucleotide changes in the CVB3/0 genome, changing an avirulent virus to a virulent one (Beck et al., 1996~.
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Therefore, the following model is proposed: Inadequate host nutrition Inadequate immune response ~ Virus Increased susceptibility to infectious disease Illness This model takes into account not only the effect that host nutriture has on the immune response but also the effect of host nutriture on the viral pathogen. This model more accurately represents the relationship between nutrition and infectious disease.
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The immune parameters that are examined need to be correlated with incidence and/or severity of infectious disease. This author recommends that any food supplement tested In military personnel for its effect on immune Unction should also be rarefied for protection against illness.
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1992. Oxidant stress alters Na+ pump and Na+K+Clcotransporter activities in vascular endothelial cells.
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1981. Copper deficiency suppresses the immune response of mice.
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1993. Effect of copper deficiency on tissue, blood characteristics, and immune functions of calves challenged with infectious bovine Rhino~acheitis virus and Pasteruella hemolytica.
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What we think is happening is that the RNA viruses have a high mutation rate because they don't have repair mechanisms. So, when they replicate, if they make a mistake, they cannot fix it, and what I think is happening is we are driving the evolution of the virus by causing the immune deficiency.
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TRACE MINERALS, IMMUNE FUNCTION, AND VIRAL EVOLUTION 357 think that nutrition can be one mechanism for driving those changes. So, I think that is a strong possibility, and clearly people I mean I am not an HIV expert, and you probably know better than I do-but I mean towards the end you see a lot of malnutrition and wasting-type syndromes in those people with HIV, and I think that can contribute to what we are seeing with the Coxsackievirus.
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358 MELINDA A BECK Now, my understanding though is Coxsackieviruses often feel like a bad cold, and so, rhinoviruses cause 40 percent of the common cold, and then there is a host of other viruses that cause similar symptoms.
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G RICHARD JANSEN: I am talking about the virulent strain.
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