March 27 (HealthDay News) -- Researchers have identified a potential new target in the ongoing quest for a treatment, and possibly a cure, for the herpes virus.
A viral protein known as VP16 is apparently responsible for pushing herpes out of its latent state and back into an active infectious state.
Experts estimate that 70 percent to 90 percent of people worldwide carry the herpes virus, although not all show symptoms. "It's a huge, huge epidemic," said study author Nancy Sawtell, a researcher in the division of infectious diseases at Cincinnati Children's Hospital Medical Center. Her report appears in the March 26 issue of PLoS Pathogens.
Herpes is transmitted by close person-to-person contact, often through the mouth or genitals. This study looks specifically at herpes simplex 1, which can cause cold sores and genital lesions. The virus can also cause stromal keritis, the leading cause of infectious blindness.
After infection at the skin surface, the virus travels to nerve cells, where it becomes dormant. Although the virus is infectious while it is replicating at the surface, it is non-infectious during this latent phase.
"About one-quarter of neurons contain latent virus," Sawtell explained. "Periodically, in response to stress, the virus will reactivate. From animal models, we know that the number of neurons that exit latency are very few, about one or two out of 6,000, and these neurons go back to the surface and replicate, potentially spreading the virus."
Scientists have long been mystified by one aspect of this ubiquitous virus: what causes it to exit the latent stage and become infectious again?
"We have been trying to understand the molecular mechanism which regulates entry into the latent cycle, what turns on the latent program, and how does that exit from latent program occur, in an effort to begin to understand how we can control that," Sawtell said.
VP16 is known to be important for starting the lytic, or reproductive, cycle upon infection of a cell. However, "it has been dogma that VP16 is not involved in reactivation from the dormant stage," Sawtell said.
But in this study, which used a mouse model, production of VP16 was a prerequisite for the virus's reactivation.
"Further," Sawtell explained, "latency in the nervous system is favored because VP16 is not transported efficiently to the nerve cell nucleus."
"There's evidence that it's not transported efficiently. VP16 is likely to be left behind, which promotes the establishment of latency," Sawtell said.
In essence, the herpes virus uses VP16 to balance the lytic and dormant stages of its life cycle.
In a second study, this one appearing recently in the online issue of Nature Immunology, a team of Canadian and U.S. researchers say they've discovered one way that the immune system activates itself to hunt down type 1 herpes.
The authors stated that the findings may one day have implications in the fight against HIV and even cancer, in addition to herpes.
SOURCES: Nancy Sawtell, Ph.D., researcher, division of infectious diseases, Cincinnati Children's Hospital Medical Center; March 23, 2009, news release, University of Montreal, Canada; March 26, 2009, PLoS Pathogens