The first comes from the recent dramatic discovery that a selenium deficiency in a person or animal triggers a mutation in the coxsackie virus. The common form of this virus is generally benign, causing symptoms no more serious than a common cold or sore throat. The coxsackie virus 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 coxsackie virus, 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 coxsackie virus 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 coxsackie virus mutation. By comparing the genetic structure of the benign "parent" coxsackie virus to that of its virulent descendants, Beck and Levander identified six specific changes in the genetic structure of the virulent coxsackie virus 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 coxsackie virus. (Nature Medicine, May 1995;1:433-6.)

The Coxsackie virus 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."

http://www.thenutritionreporter.com/selenium.html
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.