Herpes is a viral infection characterized by the development of painful blisters and ulcers. It is primarily caused by the herpes simplex virus type 1 (HSV-1), which can present with flu-like symptoms, as well as sensations of numbness, pain, and burning. A recent investigation led by Dr. Anna Cliffe from the University of Virginia has revealed that the herpes virus can manipulate the immune system that is meant to combat it, resulting in the reactivation of the virus.

The World Health Organization reports that over 60% of individuals under the age of 50 are carriers of the herpes virus, which can lead to lifelong infections within nerve cells. Once the virus infiltrates the body, it remains indefinitely. Nevertheless, the immune system can often keep the virus in check, resulting in the absence of symptoms in many individuals. However, factors such as stress, sunburn, and other infections can trigger outbreaks.

Dr Anna Cliffe, from the Department of Microbiology, Immunology, and Cancer Biology at UVA, stated, “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.”

Findings of the study:

The research identified a viral protein designated as UL12.5. The investigators noted that this protein functions as a double agent, initiating the body's antiviral response while simultaneously manipulating this response to reactivate the virus within the host.

This study calls into question the established understanding of the interaction between viruses and the immune system. Traditionally, it has been recognized that viruses attempt to evade or inhibit immune responses. However, the researchers found that the herpes virus actively seeks to take advantage of specific immune pathways by activating them.

Researcher Patryk Krakowiak informed StudyFinds, “Our team was taken aback to discover that HSV-1 does not merely remain dormant until favourable conditions arise for reactivation; rather, it actively monitors its environment for potential threats and manages the reactivation process. The results of our study indicate that the virus may utilize immune signals to identify cellular stress—stemming from neuron damage, infections, or other dangers—as a trigger to leave its current host in search of a new one.”

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