The secret of how the cold sore virus manages to persist for a lifetime in the human body may have been cracked by US scientists.

It has been long known that the herpes simplex virus 1 (HSV-1) lies dormant in facial nerves, emerging periodically and causing sores, usually when the immune system of the infected person is down.

A team of researchers from Duke University Medical Center has uncovered the way the virus reactivates itself from this dormant state.

The finding has the potential to lead to new treatments.

When fighting a virus, the immune system relies heavily on the protein chemicals produced by the virus which it uses to help mark it for destruction. Herpes viruses manage to evade the immune system by shutting down production of these proteins completely, and remaining in this state for long periods before starting to replicate again. This is why the symptoms such as cold sores and genital herpes flare-up and a patient can never get rid of the infection.

Scientists have found that there is, in fact, something that HSV-1 does produce. It is a type of RNA, a single strand of genetic information copied from the DNA of the virus. The Duke University team suspected that it somehow helps keep the virus in its dormant state and decided to study what happened to these "latent RNAs" in mice.

They get broken down into even smaller strands, called microRNAs, and block the production of proteins which reactivate the virus. This way, they were helping with keeping the virus in its dormant state.

The study author said they had provided a molecular understanding of how HSV-1 hides and then switches back and forth between the latent and active phases. He believes that a drug based on blocking these microRNAs could in theory "wake up" all the viruses and make them vulnerable to antiviral therapy.

This finding raises the possibility of a cure for herpes.

The next step in the research is to figure out what happens in animals when using a virus engineered to block production of these RNAs.