Scientists have a new target to prevent cold sores after University of Virginia School of Medicine researchers discovered an unexpected way the herpes virus re-activates in the body. The finding could also have important implications for genital herpes caused by the same virus.
The discovery from UVA’s Anna Cliffe, PhD, and colleagues seems to defy common sense. She and her team found that the slumbering herpes virus will make a protein to trigger the body’s immune response as part of its escape from dormancy. You’d think this would be bad for the virus – that activating the body’s antiviral defenses would be like poking a bear. But, instead, it’s the opposite: The virus highjacks the antiviral process in infected neurons (nerve cells) to make the type of comeback nobody wants.
Our findings identify the first viral protein required for herpes simplex virus to wake up from dormancy, and, surprisingly, this protein does so by triggering responses that should act against the virus. This is important 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.”
Anna Cliffe, PhD, UVA’s Department of Microbiology, Immunology and Cancer Biology
Understanding herpes simplex virus-associated disease
Cold sores are caused primarily by herpes simplex virus 1 (HSV-1), one of two forms of the herpes virus. HSV-1 is very contagious, and more than 60% of people under 50 have been infected worldwide, the World Health Organization