nigma
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- Dec 14, 2013
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Been reading on this topic, see below papers, links.
Is Selenium Deficiency Behind Ebola, AIDS and Other Deadly Infections?
by Jack Challem
Is Selenium Deficiency Behind Ebola, AIDS and Other Deadly Infections?
Selenium and Viral Mutations
So far, there are three pieces to the selenium-virus puzzle.
The first comes from the recent dramatic discovery that a selenium deficiency in a person or animal triggers a mutation in the coxsackievirus. The common form of this virus is generally benign, causing symptoms no more serious than a common cold or sore throat. The coxsackievirus mutation, however, attacks heart tissue, causing Keshan disease (a type of cardiomyopathy) and heart failure.
In China, Keshan disease is known to be associated with selenium deficiency. But because of the seasonal nature of Keshan disease, researchers suspected that an infectious microorganism was also involved. That's when they turned up the coxsackievirus, which also infects an estimated 20 million Americans annually.
The plot twisted last year when Melinda Beck, Ph.D., a virologist at the University of North Carolina, and Orville Levander, Ph.D., a nutritional chemist at the USDA's Agricultural Research Service, described how a run-of-the-mill coxsackievirus mutated into the deadly, rapidly reproducing strain when an infected person or animal was deficient in selenium or vitamin E. The coxsackievirus in animals eating a selenium-rich diet did not mutate. However, the mutated virus could infect and be deadly to a person or animal eating adequate selenium. (Journal of Medical Virology, 1994;43:66-70 and Journal of Nutrition, 1994;124:345-58.)
***
Review: Micronutrient Selenium Deficiency Influences Evolution of Some Viral Infectious Diseases
Review: Micronutrient Selenium Deficiency Influences Evolution of Some Viral Infectious Diseases
Abstract
Recently emerged viral infectious diseases (VIDs) include HIV/AIDS, influenzas H5N1 and 2009 H1N1, SARS, and Ebola hemorrhagic fevers. Earlier research determined metabolic oxidative stress in hosts deficient in antioxidant selenium (Se) (<1 μMol Se/L of blood) induces both impaired human host immunocompetence and rapidly mutated benign variants of RNA viruses to virulence. These viral mutations are consistent, rather than stochastic, and long-lived. When Se-deficient virus-infected hosts were supplemented with dietary Se, viral mutation rates diminished and immunocompetence improved. Herein is described the role of micronutrient Se deficiency on the evolution of some contemporary RNA viruses and their subsequent VIDs. Distinguishing cellular and biomolecular evidence for several VIDs suggests that environmental conditions conducive to chronic dietary Se deprivation could be monitored for bioindicators of incipient viral virulence and subsequent pathogenesis.
***
Selenium and host defense towards viruses
https://www.cambridge.org/core/serv...selenium_and_host_defence_towards_viruses.pdf
***
Selenium, Selenoproteins and Viral Infection
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769590/pdf/nutrients-11-02101.pdf
Abstract:Reactive oxygen species (ROS) are frequently produced during viral infections. Generation ofthese ROS can be both beneficial and detrimental for many cellular functions. When overwhelmingthe antioxidant defense system, the excess of ROS induces oxidative stress. Viral infections lead todiseases characterized by a broad spectrum of clinical symptoms, with oxidative stress beingone of their hallmarks.In many cases, ROS can, in turn, enhance viral replication leadingto an amplification loop. Another important parameter for viral replication and pathogenicityis the nutritional status of the host. Viral infection simultaneously increases the demand formicronutrients and causes their loss, which leads to a deficiency that can be compensated bymicronutrient supplementation. Among the nutrients implicated in viral infection, selenium (Se) hasan important role in antioxidant defense, redox signaling and redox homeostasis. Most of biologicalactivities of selenium is performed through its incorporation as a rare amino acid selenocysteinein the essential family of selenoproteins. Selenium deficiency, which is the main regulator ofselenoprotein expression, has been associated with the pathogenicity of several viruses. In addition,several selenoprotein members, including glutathione peroxidases (GPX), thioredoxin reductases(TXNRD) seemed important in different models of viral replication. Finally, the formal identificationof viral selenoproteins in the genome of molluscum contagiosum and fowlpox viruses demonstratedthe importance of selenoproteins in viral cycle.
***
Dietary Selenium in Adjuvant Therapy of Viral and Bacterial Infections
Dietary Selenium in Adjuvant Therapy of Viral and Bacterial Infections
Abstract
Viral and bacterial infections are often associated with deficiencies in macronutrients and micronutrients, including the essential trace element selenium. In selenium deficiency, benign strains of Coxsackie and influenza viruses can mutate to highly pathogenic strains. Dietary supplementation to provide adequate or supranutritional selenium supply has been proposed to confer health benefits for patients suffering from some viral diseases, most notably with respect to HIV and influenza A virus (IAV) infections. In addition, selenium-containing multimicronutrient supplements improved several clinical and lifestyle variables in patients coinfected with HIV and Mycobacterium tuberculosis. Selenium status may affect the function of cells of both adaptive and innate immunity. Supranutritional selenium promotes proliferation and favors differentiation of naive CD4-positive T lymphocytes toward T helper 1 cells, thus supporting the acute cellular immune response, whereas excessive activation of the immune system and ensuing host tissue damage are counteracted through directing macrophages toward the M2 phenotype. This review provides an up-to-date overview on selenium in infectious diseases caused by viruses (e.g., HIV, IAV, hepatitis C virus, poliovirus, West Nile virus) and bacteria (e.g., M. tuberculosis, Helicobacter pylori). Data from epidemiologic studies and intervention trials, with selenium alone or in combination with other micronutrients, and animal experiments are discussed against the background of dietary selenium requirements to alter immune functions.
Is Selenium Deficiency Behind Ebola, AIDS and Other Deadly Infections?
by Jack Challem
Is Selenium Deficiency Behind Ebola, AIDS and Other Deadly Infections?
Selenium and Viral Mutations
So far, there are three pieces to the selenium-virus puzzle.
The first comes from the recent dramatic discovery that a selenium deficiency in a person or animal triggers a mutation in the coxsackievirus. The common form of this virus is generally benign, causing symptoms no more serious than a common cold or sore throat. The coxsackievirus mutation, however, attacks heart tissue, causing Keshan disease (a type of cardiomyopathy) and heart failure.
In China, Keshan disease is known to be associated with selenium deficiency. But because of the seasonal nature of Keshan disease, researchers suspected that an infectious microorganism was also involved. That's when they turned up the coxsackievirus, which also infects an estimated 20 million Americans annually.
The plot twisted last year when Melinda Beck, Ph.D., a virologist at the University of North Carolina, and Orville Levander, Ph.D., a nutritional chemist at the USDA's Agricultural Research Service, described how a run-of-the-mill coxsackievirus mutated into the deadly, rapidly reproducing strain when an infected person or animal was deficient in selenium or vitamin E. The coxsackievirus in animals eating a selenium-rich diet did not mutate. However, the mutated virus could infect and be deadly to a person or animal eating adequate selenium. (Journal of Medical Virology, 1994;43:66-70 and Journal of Nutrition, 1994;124:345-58.)
***
Review: Micronutrient Selenium Deficiency Influences Evolution of Some Viral Infectious Diseases
Review: Micronutrient Selenium Deficiency Influences Evolution of Some Viral Infectious Diseases
Abstract
Recently emerged viral infectious diseases (VIDs) include HIV/AIDS, influenzas H5N1 and 2009 H1N1, SARS, and Ebola hemorrhagic fevers. Earlier research determined metabolic oxidative stress in hosts deficient in antioxidant selenium (Se) (<1 μMol Se/L of blood) induces both impaired human host immunocompetence and rapidly mutated benign variants of RNA viruses to virulence. These viral mutations are consistent, rather than stochastic, and long-lived. When Se-deficient virus-infected hosts were supplemented with dietary Se, viral mutation rates diminished and immunocompetence improved. Herein is described the role of micronutrient Se deficiency on the evolution of some contemporary RNA viruses and their subsequent VIDs. Distinguishing cellular and biomolecular evidence for several VIDs suggests that environmental conditions conducive to chronic dietary Se deprivation could be monitored for bioindicators of incipient viral virulence and subsequent pathogenesis.
***
Selenium and host defense towards viruses
https://www.cambridge.org/core/serv...selenium_and_host_defence_towards_viruses.pdf
***
Selenium, Selenoproteins and Viral Infection
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6769590/pdf/nutrients-11-02101.pdf
Abstract:Reactive oxygen species (ROS) are frequently produced during viral infections. Generation ofthese ROS can be both beneficial and detrimental for many cellular functions. When overwhelmingthe antioxidant defense system, the excess of ROS induces oxidative stress. Viral infections lead todiseases characterized by a broad spectrum of clinical symptoms, with oxidative stress beingone of their hallmarks.In many cases, ROS can, in turn, enhance viral replication leadingto an amplification loop. Another important parameter for viral replication and pathogenicityis the nutritional status of the host. Viral infection simultaneously increases the demand formicronutrients and causes their loss, which leads to a deficiency that can be compensated bymicronutrient supplementation. Among the nutrients implicated in viral infection, selenium (Se) hasan important role in antioxidant defense, redox signaling and redox homeostasis. Most of biologicalactivities of selenium is performed through its incorporation as a rare amino acid selenocysteinein the essential family of selenoproteins. Selenium deficiency, which is the main regulator ofselenoprotein expression, has been associated with the pathogenicity of several viruses. In addition,several selenoprotein members, including glutathione peroxidases (GPX), thioredoxin reductases(TXNRD) seemed important in different models of viral replication. Finally, the formal identificationof viral selenoproteins in the genome of molluscum contagiosum and fowlpox viruses demonstratedthe importance of selenoproteins in viral cycle.
***
Dietary Selenium in Adjuvant Therapy of Viral and Bacterial Infections
Dietary Selenium in Adjuvant Therapy of Viral and Bacterial Infections
Abstract
Viral and bacterial infections are often associated with deficiencies in macronutrients and micronutrients, including the essential trace element selenium. In selenium deficiency, benign strains of Coxsackie and influenza viruses can mutate to highly pathogenic strains. Dietary supplementation to provide adequate or supranutritional selenium supply has been proposed to confer health benefits for patients suffering from some viral diseases, most notably with respect to HIV and influenza A virus (IAV) infections. In addition, selenium-containing multimicronutrient supplements improved several clinical and lifestyle variables in patients coinfected with HIV and Mycobacterium tuberculosis. Selenium status may affect the function of cells of both adaptive and innate immunity. Supranutritional selenium promotes proliferation and favors differentiation of naive CD4-positive T lymphocytes toward T helper 1 cells, thus supporting the acute cellular immune response, whereas excessive activation of the immune system and ensuing host tissue damage are counteracted through directing macrophages toward the M2 phenotype. This review provides an up-to-date overview on selenium in infectious diseases caused by viruses (e.g., HIV, IAV, hepatitis C virus, poliovirus, West Nile virus) and bacteria (e.g., M. tuberculosis, Helicobacter pylori). Data from epidemiologic studies and intervention trials, with selenium alone or in combination with other micronutrients, and animal experiments are discussed against the background of dietary selenium requirements to alter immune functions.
