JUNE 15, 2001


The Straits Times
Malnutrition can spawn new global threat

A study showing that mild viruses in selenium-deficient mice can mutate into virulent forms may be a warning on the dangers of human malnutrition

By R. Senthilnathan

LACK of healthy food can ravage people, but now researchers claim it can also lead to a new form of global threat - the evolution and spread of deadly flu viruses from which even healthy people are not immune.

Scientists from Switzerland and the United States say that an inadequate intake of a mineral called selenium, a result of poor nutrition, can turn harmless strains of flu viruses into ones so virulent that they could even infect well-fed, healthy people.


'Poor nutritional status in the host may contribute to the emergence of new viral strains,' say the scientists from the Swiss-based Nestle Research Centre, the US-based University of North Carolina and the US Department of Agriculture.

Selenium (Se) is a mineral vital for life that is found in minute amounts in the human body. Among other things, it contributes to the efficient functioning of the immune system.

Plant foods, such as Brazil nuts, walnuts, rice and wheat, are the major sources of Se as they absorb it from the soil.

Parts of China and Russia have Se-deficient soils, and people there have Se-deficiency.

Earlier studies have shown that mild versions of flu, such as the Influenza A/Bangkok type, can cause severe lung infections in those with Se-deficiency.

Influenza, which is an acute respiratory illness, has caused immense suffering to mankind since time immemorial. In 1918, a worldwide flu epidemic, called Spanish Flu, killed over 40 million people.

According to the Geneva-based World Health Organisation (WHO), the Asian Flu of 1957 and Hongkong Flu of 1968 killed a total of 1.5 million people and caused damages estimated at US$32 billion (S$58 billion). It says 'hundreds of thousands' of people die from flu each year.

The present study, which has been published in the Federation of American Societies for Experimental Biology journal, expands on the earlier ones by studying how and why the viruses mutated.

One group of mice was fed with Se-adequate food and a second group with se-deficient food.

When a third group of Se-adequate mice was exposed to mutated viruses from the second group of mice, it was affected with severe lung inflammation.

This shows, says Ms Melinda A. Beck, a team member and an associate professor of paediatrics at the University of North Carolina, that once the mutations occur, it does not matter what a person's selenium status is.

'Now the Se-adequate mice will get just as sick as the Se-deficient mice when infected with the newly mutated virus,' said Ms Beck.

Even though the test results are from mice, the scientists feel the same theory applies to humans and other animals as well.

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