By Amanda Gardner
FRIDAY, Oct. 24 (HealthDay News) -- It may not be the cure for the common cold, but it may set the stage for a cure.
Canadian and U.S. researchers have found that the human rhinovirus, long blamed for causing the common cold, doesn't actually cause those annoying sniffles, sneezes, and coughs.
Instead, the ubiquitous virus alters genes in the body, which then results in the misery that afflicts most people every year or so, according to a study in the first November issue of the American Journal of Respiratory and Critical Care Medicine.
"This is like the Wizard of Oz, showing what's going on behind the curtain, what the body is doing when there's a cold," said Dr. Ronald Kuppersmith, a clinical assistant professor of family and community medicine at Texas A&M Health Science Center College of Medicine, who was not involved with the research.
"This may provide opportunities to modify the body's response to the rhinovirus and provide opportunities for further research or possibly medication that would significantly reduce the symptoms and maybe even prevent infection in a much more targeted way," he added.
Human rhinovirus (HRV) causes some 30 percent to 50 percent of common colds and can also worsen more serious conditions, such as asthma.
"Everyone thinks the common cold is fairly innocuous, which it is. But if you have people with lower airway disease -- asthma, bronchitis, emphysema -- these viruses are now known to be very important triggers for people to have acute attacks and that can be life-threatening," said David Proud of the University of Calgary, the study's lead author and a professor of physiology and biophysics and Canada Research Chair in Inflammatory Airway Diseases.
For the study, 35 volunteers agreed to be injected either with HRV or a sham virus. Scientists took nasal epithelial scrapings both before and after infection.
A "microarray analysis" of DNA showed no genetic changes eight hours after infection. But, after two days, about 6,500 genes had been altered, 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.
"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.
Visit the National Institute of Allergy and Infectious Diseases for more on the common cold.
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