Initially, Keshan disease was thought to be a deficiency disease alone, involving inadequate intakes of
Se and also of Mo, Mg, and thiamin. However, seasonal variations in symptoms suggested that at least one other interacting factor was likely involved. Later, an enterovirus and a Coxsackie virus (strain B4) were isolated from affected individuals. The same Coxsackie virus was able to produce severe heart pathology in mice when they were fed Se-deficient grain from Keshan endemic areas.
Coxsackie virus strain B3, when introduced into Se-deficient mice, produces a myocarditis that is similar to that of human Keshan's disease, and this virus consistently undergoes mutation at six distinct amino acid (= nucleotide) sites in the Se-deficient but not the control animals. These mutated viruses are then able to produce myocarditis even in selenium-replete control mice. Thus, the virulence change has become permanent by mutation, and the increased virulence is no longer dependent on a simultaneous lack of selenium. Comparable selenium limitation-induced mutations in influenza virus have also been shown in Se-deficient mice. It is suggested that in the presence of a low selenium supply, a normally quiescent virus may become activated by increased oxidative stress and host cell apoptosis, the mutation to increased virulence being a survival strategy by the virus.
In HIV-infected individuals, the progression to AIDS and the decline in T helper (CD4) cell counts are accompanied by a parallel decrease in blood selenium levels. Selenium deficiency appears to increase the probability of mortality in HIV-infected subjects.
Human selenium supplementation (e.g., 200 mg/ day), even in apparently selenium-replete individuals receiving a diet providing >120 mg Se/day, was able to stimulate the proliferation of activated T cells of the immune system. It elicited an enhanced response to antigen stimulation, an enhanced ability to generate cytotoxic lymphocytes, an enhanced ability to destroy tumor cells, and increased natural killer cell activity. Growth-regulatory interleukin-2 receptors on the surface of activated lymphocytes and natural killer cells became upregulated.
In a study in Liverpool, UK, healthy adult subjects with initial plasma selenium concentrations below 1.2 mmol/l were given placebo or 50 or 100 mg daily supplements of selenium as selenite for 15 weeks. After 6 weeks, they were given oral live attenuated polivirus vaccine, and after 9 weeks, 74Se stable isotope was given intravenously to measure their body Se pool size. The Se supplements significantly increased the Se pool size, and the supplemented groups cleared the poliovirus more rapidly and their fecal viral RNA products exhibited fewer mutations. Cellular immune response (estimated by interferon-7 and other cytokines) was enhanced and there was an earlier peak of T cell proliferation and numbers in the supplemented groups. This study suggests that selenium supplements can improve a number of indices of immune function, even in individuals whose Se status is not severely deficient.
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