Diet causes viral mutation in mice.
"This interesting work is the first to show that a nutritional deficiency can accelerate evolution of a virus population from benign to virulent in an intact animal," assert Charles J. Gauntt of the University of Texas Health Science Center in San Antonio and Steven Tracy of the University of Nebraska Medical Center in Omaha. Their comments appear in an editorial that accompanies the announcement in the May Nature Medicine of the findings by Melinda A. Beck of the University of North Carolina at Chapel Hill and her colleagues.
Coxsackieviruses infect more than 20 million people annually in the United States and can cause illnesses ranging from a cold to an inflammation of the heart. However, most of the viruses are benign, so only about 10,000 infected people become ill.
In previous studies, Beck and other researchers had linked coxsackievirus and heart disease to selenium intake in humans as well as mice. People deficient in the mineral tend to develop Keshan disease, an inflammatory heart disease. Scientists had found coxsackieviruses in Keshan patients, they note.
Last year, Beck and her colleagues reported their first inkling that the coxsackievirus mutates in nutritionally deprived hosts. The team found that a normally benign strain of coxsackievirus B3 (CVB3) damaged the hearts of selenium-deficient mice. Injecting virus from these animals into selenium-rich mice caused the healthy creatures to develop heart disease.
In their new study, Beck and her coworkers fed mice either a diet very low in selenium or a normal diet for 4 weeks, then injected benign CVB3 into both groups. After 7, 10, and 14 days, the scientists killed and examined 10 mice from each group. After only 7 days, the mice that lacked selenium showed signs of heart disease, including inflammation. The well-nourished mice stayed diseasefree.
The researchers compared the original virus, the virus taken from the hearts of the selenium-deficient mice, and strains of CVB3 known to cause heart disease. In the deprived mice, the original virus' sequence of nucleotides, the building blocks of ribonucleic acid (RNA), underwent six changes. These same mutations appear in the CVB3 strain that causes heart disease, Beck and her colleagues report.
They speculate that the virus changes rapidly in selenium- deficient hosts because of the animals' weakened immune systems. The mineral, an antioxidant, helps protect the immune system from the damaging by-products of normal metabolic functions. Also, coxsackieviruses and similar viruses mutate readily.
Whether the virus requires all six or only one or two of the mutations to become virulent remains unclear, the authors note. They are now investigating why the changes occur at such specific sites on the genome and what happens to the virus in animals only slightly low on selenium.
If coxsackieviruses and other viruses become virulent when they infect nutritionally deprived people, that may "help explain the steady emergence of new strains of influenza virus in China, which has widespread selenium-deficient areas," Beck's team argues.
"Our findings might even help to explain the crossing over of certain viruses [such as HIV] to a new host species through accelerated mutation rates," the authors speculate. HIV apparently first infected monkeys and then moved to some humans living in selenium-poor regions of Africa, they note.
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|Title Annotation:||selenium deficiency|
|Date:||May 6, 1995|
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