Now that researchers have found how cold sores operate, they believe they may soon discover how to eradicate the virus that causes them.

Cold sores, which usually show up as painful, ulcerated blemishes around the mouth, are caused by the herpes simplex virus (HSV1). The virus often lies dormant in a nerve in the face, called the trigeminal nerve, until activated by sunlight, a poorly functioning immune system, stressful situations or a high fever.

By examining the interplay of various molecular substances the virus produces, researchers at Duke University Medical Center in Durham, N.C., have found how it hides and then emerges periodically.

One such substance is called latency associated transcript RNA, which the study reveals blocks the formation of proteins that "turn" on the virus and make it replicate. It does this by splitting into strands of microRNAs, which essentially keep the virus in check.

However, in stressful situations, the virus makes more messenger RNA than the microRNAs can handle and eventually viral replication occurs.

"We have provided a molecular understanding of how HSV1 hides and then switches back and forth between the latent [hidden] and active phases," Bryan Cullen, Duke professor of molecular genetics and microbiology, said in a release.

The researchers believe this discovery could lead to a treatment in which the artificial activation of the virus would lead it to be killed by administering acyclovir, a medication that kills replicating HSV1. The virus cannot be treated while in a dormant state.

"In principle, you could activate and then kill all of the virus in a patient," said Cullen. "This would completely cure a person, and you would never get another cold sore."

The study is published in the June issue of the journal Nature.