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Mouse study suggests a cure for influenza.

Mouse study suggests a cure for influenza

Scientists have developed a drug that cures mice of influenza and demonstrated for the first time that influenza's symptoms are not caused directly by the virus, but instead result from the action of oxidizing free radicals produced by the immune system. The finding not only suggests a cure for the disease in humans, but also holds "great potential" for treating a number of other inflammatory diseases -- such as hepatitis, rheumatoid arthritis and Crohn's disease (a severe intestinal disorder) -- says study leader Hiroshi Maeda, a biochemist at Kumamoto University Medical School in Japan.

Previous studies have suggested an overreaction of the immune system might contribute to flu symptoms. And other work has shown that immune cells produce free radicals -- highly reactive compounds containing unpaired electrons that steal electrons from other molecules and cause tissue damage. But no one before now had demonstrated the importance of free radicals in influenza, Maeda says.

The scientists initially found that the levels of free radicals generated by immune cells taken from influenza virus-infected mouse lungs increased with time after infection. They also found T lymphocytes increased in number, suggesting that elevated free-radical production by immune cells, possibly primarily the T cells, contributes to influenza pathogenesis, Maeda says.

They then identified the enzyme, xanthine oxidase, responsible for the generation of the free radicals. Xanthine oxidase activity increased dramatically after infection in both influenza-infected mouse lung cells and infected mouse serum. Administering allopurinol, a xanthine oxidase inhibitor, "exerted a protective effect on the mice," the scientists write in the May 26 SCIENCE.

In a separate experiment, nine of 10 mice treated with a derivative of a naturally occurring free-radical scavenger survived, while all 10 controls died. The treated mice were injected daily for four days, beginning on the fifth day after infection, with a derivative of the enzyme superoxide dismutase. It was made to remain longer at the site of free-radical damage by linking it to a synthetic polymer. Treatment dramatically diminished the pathological changes within the lung, returning the mice to "almost like normal," Maeda says.

Maeda's work "opens up a whole new world of therapeutic chemistry in which one uses polymers as carriers [for drugs]," says oncologist William Regelson at Virginia Commonwealth University Medical College of Virginia in Richmond.
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Author:Wickelgren, I.
Publication:Science News
Date:May 27, 1989
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