"This provides a new strategy to use for seeking a cure," said Christopher Beisel, a virologist and program officer at the U.S. National Institute of Allergy and Infectious Diseases, which funded the Duke research. "However, I always caution people that when something like this comes out, and people start talking about cures, that there's a long way to go, starting with animal experiments."
And Beisel noted that there's always an element of risk whenever doctors purposefully re-awaken a dormant virus. "You are bringing it forth with the possibility of causing disease and then having to stomp on it before it does. So, I am cautiously optimistic, but there are some problems to work out."
Nevertheless, the findings could apply to the whole range of herpes viruses, including herpes simplex 2, which causes genital herpes, and the varicella zoster virus, which causes chickenpox and a more chronic, painful condition known as shingles.
In fact, Umbach said, the Duke group plans to target the shingles virus in their next round of research.
Beisel agreed that the findings could have implications far beyond the common cold sore.
"I'm highly psyched about this as basic research," he said. "Just being able to understand what's going on with latency may have relevance to other herpes viruses."
There's more on oral herpes at the American Social Health Association.
SOURCES: Jennifer Lin Umbach, Ph.D., postdoctoral associate, department of molecular genetics and microbiology, Duke University, Durham, N.C.; Christopher Beisel, Ph.D., program officer, U.S. National Institute of Allergy and Infectious Diseases, Bethesda, Md; July 2, 2008, Nature, online
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