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Scientists ID Gene That Predicts Chances of Cold Sores
Two variants seem to raise the risk of recurrent outbreaks, while two lower the possibility.
FRIDAY, Dec. 2 (HealthDay News) -- Scientists have identified the first gene associated with frequent herpes-related cold sores.
The herpes simplex virus type 1 (HSV-1) affects more than 70 percent of the U.S. population. Once the virus infects the body it is never removed by the immune system. It's transported to nerve cell bodies, where it remains dormant until reactivated.
A cold sore on or around the mouth is the most common visible symptom of HSV-1 reactivation.
"Researchers believe that three factors contribute to HSV-1 reactivation -- the virus itself, exposure to environmental factors and genetic susceptibility," study first author Dr. John Kriesel, a research associate professor of infectious diseases at the University of Utah School of Medicine, said in a university news release. "The goal of our investigation was to define genes linked to cold sore frequency."
He and his team conducted genetic analyses of 355 people infected with HSV-1 and 263 uninfected people and discovered that a gene called C21orf91 was associated with susceptibility to frequent cold sore outbreaks.
Two variants of the gene seemed to protect against HSV-1 reactivation while two other variants seemed to increase the risk of frequent cold sore outbreaks, according to the report published in the Dec. 1 issue of the Journal of Infectious Diseases.
"There is no cure for HSV-1 and, at this time, there is no way for us to predict or prevent cold sore outbreaks," Kriesel said in the news release. "The C21orf91 gene seems to play a role in cold sore susceptibility, and if this data is confirmed among a larger, unrelated population, this discovery could have important implications for the development of drugs that affect cold sore frequency."
The American Academy of Dermatology has more about cold sores and other mouth and lip conditions.
(SOURCE: University of Utah Health Sciences, news release, Nov. 29, 2011)
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