Explainer | Herpes virus study finds trigger for cold sore outbreaks that could lead to stopping them
New research gives hope to potentially preventing the herpes simplex 1 virus from waking up and activating immune responses in the body
Have you ever had a cold sore? They are common, uncomfortable and can be hard to get rid of. But there is new hope on the horizon.
Research has discovered that a protein in the herpes simplex virus 1 (HSV-1) – a virus that causes both cold sores and a small proportion of genital herpes, and which can lie dormant for extended periods – is required to activate the immune system and reawaken the virus when it is dormant.
When the virus reawakens, it hijacks the body’s antiviral action, allowing it to storm back with a vengeance. A fresh crop of painful sores subsequently develops.
The virus can make this protein while it lies dormant.
“This is an important finding because it gives us new ways to potentially prevent the virus from waking up and activating immune responses in the nervous system that could have negative consequences in the long term,” says Anna Cliffe, lead author of the study published by the University of Virginia School of Medicine, in the US.
Cold sores are quite contagious. The World Health Organization (WHO) estimates that 64 per cent of the global population under 50 are infected with HSV-1, some 3.8 billion people.