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U.S. scientists say they have identified the cells in the immune system that suppress outbreaks of genital herpes in infected individuals.

The discovery, published on Wednesday in the journal Nature, could lead to an effective treatment for the condition and help to prevent it from being spread to others.

The new research also fundamentally alters medical understanding of the genital infection known as the herpes simplex virus Type 2, or HSV-2. (The Type 1 version causes colds sores around the mouth.)

Once infected, the virus can't be eradicated from the body. It finds a home in nerve cells, occasionally erupting to the surface of the skin, producing painful blisters. It tends to be reactivated by such factors as illness, emotional and physical stress, fatigue and exposure to bright sunlight.

Scientists have assumed that the immune system makes a concerted effort to beat back the virus only during active outbreaks. But the new research suggests there is an almost constant struggle between the immune system and the virus.

"We have taken a snapshot of the battlefield between the virus and the host … and the body is attacking it on a pretty frequent basis," said the study's senior author, Dr. Larry Corey, director and president of the Fred Hutchinson Cancer Research Center in Seattle.

Using sophisticated cell-isolating techniques, the researchers discovered a specialized type of immune T-cell – dubbed CD8aa – around HSV-2-infected nerve cells.

"These CD8aa T-cells are essentially doing immune surveillance and making antiviral substances that keep back the virus," Corey explained.

He noted that the virus is producing copies of itself that leak into the skin "every few days, not just every once in a while." That suggests that the immune system is fighting the virus almost all the time. "Sometimes it loses the battle, but most of the time it is actually winning," Corey said.

Researchers at the Fred Hutchinson Cancer Research Center and the University of Washington first discovered the existence of the CD8aa cells in the genitalia about three years ago. The new study takes their initial work a step further by showing how these immune cells are involved in keeping genital herpes in check.

Corey speculated that the virus produces open sores on the skin where there are a limited number of CD8aa cells. "In the areas where there are lots of them, the virus would be contained. And, in areas where these cells are few and far between, the virus pops up and causes lesions."

Current herpes treatments are limited and not always effective. Patients can take antiviral medications that hinder the virus from reproducing itself. But these drugs must be taken on an ongoing basis to prevent an outbreak. And, if taken after a lesion erupts, they just shorten the time the person is infectious and speed the healing process.

The study also helps to explain why an infected person can spread the virus to a sexual partner without showing any symptoms. A few stray viruses leak through the skin in areas where there are are not many CD8aa cells.

In fact, a recent Canadian study suggests that many people unknowingly pass on genital herpes to their sexual partners. In a random sample of Canadians, nearly 14 per cent tested positive for genital herpes. Of this group, a substantial majority had no previous symptoms.

The new research could lead to better treatments, such as a vaccine to boost the number of CD8aa cells.

"I think this is good news for the public," Corey said. "Some people will be worried that herpes is reactivating all the time, but the better news is that the human immune system is able to contain it – and it gives us a tool to actually improve containment."