- Cold sores are a common sign of herpes simplex virus infection
- Sunburn and stress have long been identified as triggers that lead to cold sores
- New research provides insight into these triggers, which could help to prevent outbreaks
Findings of a recent study conducted by researchers at the University of Virginia School of Medicine could help prevent cold sores, and even eye disease caused by herpes, from recurring.
“Herpes simplex recurrence has long been associated with stress, fever and sunburn,” said Anna R Cliffe, who is one of the researchers affiliated with the study.
This study sheds light on how all these triggers can lead to herpes simplex-associated disease.
What causes cold sores?
Cold sores are painful blisters that develop on the lips, caused by the herpes simplex virus (HSV1). HSV1 is spread through contact with an infected person and this can occur through kissing a person with visible sores or in the absence of sores, when the virus is present in a person’s saliva.
Once you’re infected, the virus never goes away. Instead, it remains dormant until reactivated, resulting in a flareup where it presents itself visibly in the form of a cold sore.
Triggers for HSV1 reactivation
The researchers studied mouse neurons infected with the herpes simplex virus and, using a specially formulated model, found that the virus “hijacks” important immune functions in the body.
When undergoing stress for extended periods of time, the immune system responds by releasing a particular type of cytokine (proteins vital for immune function) known as Interleukin 1 beta. Interleukin 1 beta is also found in skin and eye cells, and is activated when these cells are damaged by sunlight.
The researchers discovered that these cytokines stimulate affected cells to a point where conditions are made optimal for a flareup to occur.
“It is really remarkable that the virus has hijacked this pathway that is part of our body’s immune response,” Cliffe said.
Targeting the virus
“It highlights how some viruses have evolved to take advantage of what should be part of our infection-fighting machinery.”
The researchers hope that these findings can assist doctors to better understand what the virus does to different neurons and the immune system, in order to prevent flareups.
“Ultimately, what we hope to do is target the latent virus itself and make it unresponsive to stimuli such as Interleukin 1 beta,” Cliffe concluded.
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