Scientists have identified a key viral protein, UL12.5, that plays a major role in triggering herpes simplex virus (HSV-1) reactivation, offering hope for new treatments. The virus, which affects over 60% of people worldwide, remains dormant in nerve cells until stress or illness causes an outbreak.
Researchers at the University of Virginia found that HSV-1 actively hijacks the immune system by triggering mitochondrial stress, which paradoxically helps the virus wake up. By targeting this viral protein, future treatments could prevent cold sores and genital herpes rather than just managing symptoms.
Current antiviral drugs can only suppress outbreaks, but this discovery could lead to therapies that stop the virus from reactivating in the first place. Scientists are now testing inhibitors to block UL12.5, which may offer a new way to control herpes infections. The study also highlights potential links between HSV-1 and neurological diseases, further emphasizing the need for better treatments.