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Page: << Prev | 1 | 2 A "microarray analysis" of DNA showed no genetic changes eight hours after infection. But, after two days, about 6,500 genes had been affected, either with heightened activity or dampened activity.
The genes most affected by the presence of the virus were ones that make antiviral proteins and pro-inflammatory chemicals that contribute to airway inflammation, the researchers said.
The researchers then found that levels of the antiviral protein with the greatest increased activity, viperin, were more than doubled in cells that had had the viperin-protein turned down, showing that HRV replication was hampered by viperin.
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"This is a previously unknown part of your body's defenses against the virus," Proud said. "[The findings] open up two major avenues. If you can identify pro-inflammatory genes that you think are the bad guys causing symptoms, you could block them. The second avenue would be identifying what are the key molecules that help fight the virus and boost their ability or supplement them with something from the outside."
"We're not curing the common cold today or tomorrow, but, hopefully, we're opening up avenues for the future," he said.
The study included researchers from the University of Virginia and the company Procter & Gamble.
A second study, this one published in the Nov. 15 issue of The Journal of Infectious Diseases, found that respiratory syncytial virus, the main cause of lung infections and hospitalizations in children, may actually linger in the body even after symptoms subside.
This could lead to chronic airway disease, such as asthma, said the investigators, from the University of Texas Southwestern Medical Center at Dallas. It could also mean a target for new treatments for children with chronic airway disease.
More information
Visit the National Institute of Allergy and Infectious Diseases for more on the common cold.
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