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A old osteoporosis drug may be effective in killing a range of influenza viruses, including ones that are very dangerous to people like the H5N1 bird flu virus, scientists in Hong Kong reported on June 27.
Unlike antiviral drugs that target and mute flu viruses, the drug pamidronate boosts a certain class of human immune cells and sets them off on a killing spree to exterminate host cells that are infected with flu viruses.
The experts, who published their findings in the Journal of Experimental Medicine, described the immune cells - called gamma-delta T-cells - as being able to recognise host cells that are infected with flu viruses. They punch holes through the membrane of the infected cells, then secrete and inject an enzyme into the cells, killing them.
"The drug activates and expands this group of T-cells, their numbers dramatically increase and they kill these virus-infected cells by secreting and injecting an enzyme," said Professor Malik Peiris, a member of the research team and leading microbiologist at the University of Hong Kong. "This drug boosts our own immune system, so the likelihood of it triggering a mutation (that results in viruses becoming resistant) is lower," said Professor Lau Yu-lung, head of pediatrics and adolescent medicine at the same university.
In their experiment, the scientists used specially bred mice which had their own immune systems removed and substituted instead with a complete set of the human immune system.
The "humanised mice" were split into three groups and infected separately with the pandemic H1N1 swine flu virus, H5N1 and H9N2 bird flu viruses.
Within each of the groups, mice that were treated with the drug recovered very quickly, while those that were not given any treatment died within a few days, said Associate Professor Tu Wenwei, also a member of the team.
Interestingly, the drug did not work on "humanised mice" that did not have these gamma-delta T-cells to begin with - which means that the drug only boosts the numbers of these T-cells, but does not create them.

Copyright Reuters, 2011

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