Jack Challem
12/04/96 The latest Ebola epidemic in Zaire may be over, but it’s probably only a matter of time before this supergerm returns – and still others emerge.
The reason: Ebola and other deadly viruses, including the human immunodeficiency virus-1 (HIV-1), might be stimulated by deficiencies in the mineral selenium.
And Zaire – where the Ebola and HIV-1 viruses first appeared – may be a viral “hot zone” because of low selenium levels in the soil and widespread selenium deficiencies among people living off that land.
Too strange to be true? To the contrary, a similar connection has been established in China, where a common virus mutates into a dangerous form when it infects people deficient in selenium.
Selenium, an essential mineral, functions as an antioxidant and a component of another antioxidant, glutathione peroxidase. Deficiencies of either substance impair the body’s immune system and ability to fight infections.
But if recent research is any indication, the role of selenium in disease prevention may be much more profound than previously imagined.
Admittedly, there’s no neat, well-documented association between selenium deficiency and the Ebola virus, but the evidence strongly suggests one.
“It is certainly intriguing that a number of viruses have emerged from these regions in Africa, which appear to be selenium deficient,” said E.
Will Taylor, Ph.D., a viral researcher at the University of Georgia, Athens.
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.)
Their research took on greater significance this past May, when Beck and Levander described the specific genetic changes that occurred in this coxsackievirus mutation. By comparing the genetic structure of the benign “parent” coxsackievirus to that of its virulent descendants, Beck and Levander identified six specific changes in the genetic structure of the virulent coxsackievirus strain. Although it’s not yet clear whether one or all of these genetic changes triggered the more aggressive virus, the genetic evidence provides the scientific proof needed to link a host’s selenium deficiency with a more dangerous form of the coxsackievirus.
(Nature Medicine, May 1995;1:433-6.)
The coxsackievirus infection is made worse because selenium deficiency weakens the host’s immunity, preventing the virus from being effectively challenged by T-cell lymphocytes or antibodies. As a result, the mutated virus can reproduce faster than it would in a relatively healthy person. In addition, the lack of selenium prevents the quenching of mutation-causing free radicals, so when the virus reproduces, it also mutates at a faster rate.
Although Beck and Levander studied only one virus, the implications are profound. They have already begun looking at whether other “host”
nutritional deficiencies cause viral mutations as well. According to Beck, this propensity to mutate in a selenium-deficient animal or person might explain why new influenza strains regularly emerge from China, where selenium deficient soils are common. The flu virus originates in Chinese ducks, jumps to pigs, and then infects people.
“The importance of this finding is not limited to nutritionally deprived populations,” the researchers said in a statement released by the USDA Agricultural Research Service. “In theory, it would take only one selenium-deficient person or animal to produce a new family of virus mutants.”
Selenium and HIV
The second piece of the Ebola-selenium puzzle comes from Taylor at the University of Georgia, Athens. Last year, he theorized that several little-known genes in HIV control the formation of selenocysteines, proteins with a voracious appetite for selenium.
When the virus depletes all of the selenium in an HIV-infected cell, it reproduces and begins attacking other cells in search of more selenium. The more selenium the virus uses, the less that’s available for the body’s immune system. Eventually, immunity becomes so weak that AIDS patients become vulnerable to life-threatening “opportunistic” infections. (Journal of Medicinal Chemistry, Aug. 19, 1994;37:2637-54.)
If the theory is correct, supplemental selenium would do two things, Taylor said in an interview. First, it would provide what the HIV virus needs so it wouldn’t spread throughout, creating a biochemical stalemate of sorts.
Second, it would help keep the person’s overall immune system functioning, so it could resist the secondary infections that usually kill HIV patients.
Genetic evidence and clinical studies using selenium in the treatment of AIDS suggest that the theory is true. In one ongoing study, Juliane Sacher, M.D., of Frankfurt, Germany, reported that selenium-supplemented AIDS patients gain weight, have a general feeling of well-being, and sometimes benefit from increases in protective CD4 T-cells. (Chemico-Biological Interactions, 1994; 91:199-205.) Another study has found that selenium inhibits the growth of HIV-1 in the test tube. (Taylor EW, Antiviral Research, 1995;26:A271-86.)
The Selenium-Ebola Link
The third piece of the Ebola-selenium puzzle comes from a recent paper Taylor has submitted for publication. In it, he draws on his earlier work and that of Beck and Levander to build a compelling argument that Ebola also contains genes dependent on selenium. Like HIV, when selenium levels in Ebola-infected cells drop, or are low to begin with, the virus reproduces and “escapes” in search of cells with more selenium-spreading the infection throughout the body.
The difference is that the genes in the Zaire strain of Ebola genes appear to need 10 times more selenium than does HIV, and Ebola’s greater dependence on selenium may partly account for the speed with which it kills. Seventy-five percent of the people infected with Ebola die within three weeks.
Again, compounding the infection, normal immune defenses against to the virus would be handicapped if the host – an animal or person – were deficient in selenium. “This raises the possibility that selenium deficiency in host populations may actually foster viral replication, possibly triggering outbreaks and perhaps even facilitating the emergence of more virulent viral strains,” explained Taylor.
It’s all very speculative, he admits. But the widespread soil deficiency of selenium in Zaire, documented by a number of researchers, would set the stage for vital mutation and a highly susceptible population, much the way it does in China.
But there’s still another aspect, Taylor points out. Sulfur dioxide, a byproduct of the burning of fossil fuels, reacts with selenium compounds in the soil, making the mineral more difficult to absorb by plants. “It has long been suspected that fossil fuel burning and acid rain may be contributing to a gradual decrease of selenium in the food chain,” Taylor said. “Thus, the deforestation of jungles and rain forests-exactly what is being done in Zaire and elsewhere-may also contribute to the emergence of new viral diseases.
This article originally appeared in the Natural Foods Merchandiser, published by New Hope Communications. The information provided by Jack Challem and The Nutrition Reporter newsletter is strictly educational and not intended as medical advice. For diagnosis and treatment, consult your physician.
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