RESEARCHERS who mapped the DNA of more than 100 different cold viruses said recently they have discovered a shortcut in their life cycle, which may explain why they can inflict misery so quickly.
They also believe they may be able to design drugs to fight the rhinoviruses, 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.
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 it gets chopped up.
“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.
Liggett’s team also found the viruses take a shortcut in making the proteins, which probably speeds up their ability to make a person feel sick soon after infection.