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Wan LixinOpinion deputy editor of Shanghai Daily
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DNA map may help find the cold cure
Source: Agencies |
February 14, 2009, Saturday
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Print Edition
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RESEARCHERS who mapped the DNA of more than 100 different cold viruses said they may find ways to design better drugs to fight the virus, which use their single gene to move rapidly from person to person, causing symptoms that range from irritating sniffles to pneumonia.
Instead of designing one drug to cure the common cold, several may be needed because the virus mutates so efficiently, said Dr Stephen Liggett of the University of Maryland medical school, who led the study published in the journal Science.
"We may end up having four or five drugs," Liggett said on Thursday.
The hope had been that it might be easy to fight the viruses, which sicken children on average 10 times a year and adults at least twice a year on average.
This is because any rhinovirus has just one gene, which in turn makes a giant protein that appears to do little or nothing until it gets chopped up into 11 smaller pieces by an enzyme called a protease.
Researchers tried to attack this big, clumsy protein before. "The first drug, the virus mutated around it," Liggett said.
"But now that we have all the pieces we can begin to understand what areas are not so flexible. We can begin to do some more rational drug design."
For example, it might be possible to attack the protease - an approach that has worked in fighting AIDS. "If we could inhibit that protease from cleaving that protein, maybe we could render all rhinoviruses ineffective," Liggett said.
The viruses also swap genes promiscuously in the equivalent of viral sex, a process known as recombination. This helps them constantly change and adapt.
Instead of designing one drug to cure the common cold, several may be needed because the virus mutates so efficiently, said Dr Stephen Liggett of the University of Maryland medical school, who led the study published in the journal Science.
"We may end up having four or five drugs," Liggett said on Thursday.
The hope had been that it might be easy to fight the viruses, which sicken children on average 10 times a year and adults at least twice a year on average.
This is because any rhinovirus has just one gene, which in turn makes a giant protein that appears to do little or nothing until it gets chopped up into 11 smaller pieces by an enzyme called a protease.
Researchers tried to attack this big, clumsy protein before. "The first drug, the virus mutated around it," Liggett said.
"But now that we have all the pieces we can begin to understand what areas are not so flexible. We can begin to do some more rational drug design."
For example, it might be possible to attack the protease - an approach that has worked in fighting AIDS. "If we could inhibit that protease from cleaving that protein, maybe we could render all rhinoviruses ineffective," Liggett said.
The viruses also swap genes promiscuously in the equivalent of viral sex, a process known as recombination. This helps them constantly change and adapt.
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