The problem with herpes viruses is that one infection isn't enough. After the initial infection, the virus enters neurons and hides, occasionally escaping from this period of latency to cause a flare-up of the disease. Now, however, researchers have a good clue as to why the virus recurs.
In studies in mice, researchers identified a viral protein, called VP 16, that appears to be the key to the dormancy and reactivation of the virus. Researchers at Cincinnati Children's Hospital Medical Center and the University of Cincinnati College of Medicine caused a high fever in a mouse with herpes. Certain triggers, such as fever, are known to cause herpes to reactivate. The researchers found that VP 16 must be produced before the virus can leave the neuron and reactivate. The study is published in the journal PLoS Pathogens.
"This completely changes our thinking about how this virus reactivates from latency," said Richard Thompson, a co-author of the paper and researcher at the University of Cincinnati, in a news release. "Instead of a simple positive switch that turns the virus on following stress, it appears instead to be a random de-repression of VP 16 gene that results in reactivation."
Knowing this should help researchers devise ways to prevent the virus. There is no treatment to eliminate herpes from the body or prevent it from reactivating although antiviral medications can help prevent outbreaks and stop the spread of the disease to some degree.
-- Shari Roan
Photo credit: Advanced Cell Technology Inc.