The herpes virus, as it spreads and causes small blisters on the skin, goes through a sorting step, making it vulnerable to treatment, new research suggests. Scientists looked at the herpes simplex virus type 1 (HSV-1), which many people contract during childhood. It hides inside nerve cells and can remain dormant for years before reaching skin cells and causing cold sores.

The researchers found that while hundreds of viral particles can dormant inside nerve cells, only one or two of them will enter the skin cells and begin to act, multiplying and spreading to other skin cells, creating a skin rash.

This moment is like the bottleneck where the infection is most susceptible to drug therapy. However, laboratory studies still need to be validated by animal and human testing to be able to confidently apply the knowledge gained to treatment. 

Currently, there is no cure for HSV-1 infection. Anti-inflammatory drugs can temporarily relieve symptoms, but they don’t target the virus itself. (HSV-1 can also cause genital herpes, although in most cases it is caused by the corresponding herpes simplex virus type 2).

The results of the study also shed light on why the herpes virus is such an effective pathogen – after all, only the strongest viruses spread from nerve cells to the surface of the skin, and then to other people. Imperfect viral particles are unlikely to survive such a journey.

The researchers believe their findings could apply to viruses similar to HSV-1, such as chickenpox, but more research is needed to confirm this.