New Study Shows How Herpes Virus ‘Hijacks’ The Immune System To Survive

Herpes is a common viral infection that causes painful blisters and ulcers. It is caused by the herpes simplex virus-1 (HSV-1) and can lead to flu-like symptoms, numbness, pain, and a burning sensation in affected areas. While the body’s immune system can keep the virus suppressed, a new study led by Dr Anna Cliffe from the University of Virginia has found that the herpes virus can hijack the same immune system that fights it—causing reactivation.

Herpes Infection

According to the World Health Organization (WHO), more than 60 per cent of people under the age of 50 carry the herpes virus. Once the virus enters the body, it remains in the nerve cells for life. Many people may never experience symptoms because the immune system keeps the virus dormant. However, certain triggers like stress, sunburn, infections, or a weakened immune system can cause it to flare up, leading to painful outbreaks.

Common Symptoms of Herpes

While some people with herpes may not show symptoms, others can experience:

New Research Sheds Light on Reactivation

Dr Anna Cliffe, from UVA’s Department of Microbiology, Immunology, and Cancer Biology, explains how the virus reactivates. She said, “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.”

How the Virus Hijacks the Immune System

The study focused on a viral protein called UL12.5. Researchers found that this protein acts as a "double agent." Instead of simply hiding from the immune system like most viruses, herpes virus actually activates the body’s antiviral alarm. It then manipulates this alarm to reactivate itself inside the body.

Traditionally, viruses are known to evade or suppress immune responses to survive. However, this study suggests that HSV-1 does something different—it uses immune signals to detect stress in the body. When it senses cellular damage, infections, or other threats, it takes this as a cue to reactivate and spread to new hosts.

Researcher Patryk Krakowiak told StudyFinds, “We were surprised to find that HSV-1 doesn’t just passively wait for the right conditions to reactivate – it actively senses danger and takes control of the process. Our findings suggest that the virus may be using immune signals as a way to detect cellular stress – whether from neuron damage, infections or other threats – as a cue to escape its host and find a new one.”

What This Means for Herpes Treatment

This groundbreaking research challenges what scientists previously knew about how viruses and the immune system interact. Understanding how HSV-1 reactivates could open new doors for treatment. If researchers can find ways to block the viral protein UL12.5, they may be able to prevent herpes reactivation—reducing outbreaks and transmission.

As scientists continue to study the herpes virus, this discovery could pave the way for better treatments and possibly a vaccine in the future.

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