A new scientific breakthrough maybe able to keep the herpes virus in a dormant, harmless stage, said researchers at Cincinnati Children’s Hospital Medical Center in a report for a recent issue of PLoS Pathogens magazine that was summarized by Health.com.
The virus travels to different human carriers via close contact, usually through the mouth or genitals. The hospital’s study focused on a variant of herpes that causes cold sores and genital lesions, called herpes simplex 1.That strain of herpes is also responsible for the number one cause of infectious blindness.
Once the virus infects the skin, it moves to cells in the nerves and lies inactive. This is called the latent phase of the virus’s life cycle.
"About one-quarter of neurons contain latent virus," said Nancy Sewtell, one of the study’s researchers. "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 know that much, but have never been able to figure out what triggers latent cells to become infectious. "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," said Nancy.
VP16, a viral protein, causes herpes to move from the inactive phase to an infectious stage, according to the study. Using a test mouse, scientists were able to prove that VP16 was an important part of the herpes virus becoming dangerous, a fact that had previously been disbelieved.
"It has been dogma that VP16 is not involved in reactivation from the dormant stage," said Nancy. She found that creation of the protein VP16 was required for the virus to reproduce.
"Further," Nancy explained, "latency [when the virus is dormant] 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,” Nancy said.
So, what Nancy found out is that herpes in the body uses the protein VP16 to balance its cycle of dormancy and activity. This info is extremely important because between 70 and 90 percent of humans around the globe are carriers of herpes, though some are asymptomatic. "It’s a huge, huge epidemic," said Nancy.
The researchers hope that their work will not only help herpes sufferers, but also shed light on HIV and maybe cancer.
– Whitney Teal