New study sheds light on the causes of cold sores and herpes outbreaks

New study sheds light on the causes of cold sores and herpes outbreaks

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A revolutionary discovery about the causes of herpes outbreaks by researchers at the University of Virginia School of Medicine may provide new ways to prevent recurrent herpes-related wounds and eye diseases.

The study, published on Wednesday in the scientific journal eLife, appears to have discovered the operating mechanism that causes things like stress, fever and sunburn to trigger herpes outbreaks.

“Herpes simplex recurrence has been linked to stress, fever and sunburn,” said researcher Anna R. Cliffe, PhD, from UVA’s Department of Microbiology, Immunology and Cancer Biology. “This study sheds light on how all of these triggers can lead to the disease associated with herpes simplex.”

The Herpes simplex-1 virus (HSV-1) is one of the most common human pathogens in existence, present in approximately 40-90% of the world population, producing a latent infection in neurons, which is reactivated from time to time for the rest of the a infected individual’s life.
Cold sores, also known as fever blisters, are one of the most common symptoms of HSV reactivation. However, recurrent reactivation can lead to herpes keratitis – a serious eye disease that, if left untreated, can result in blindness – and, in extreme cases, even encephalitis. HSV infection has also been linked in several studies to the progression of Alzheimer’s disease.

Cliffe and his colleagues found that when HSV-infected neurons were exposed to stimuli that induce “neuronal hyperexcitation”, the virus was able to sense the specific change and seize the opportunity to reactivate.

Working on a model developed by the Cliffe lab, which analyzes neurons infected with HSV in mice, the researchers determined that the virus essentially “hijacks” an important pathway for an immune response within the body.

In response to prolonged periods of inflammation or stress, the immune system releases a specific cytokine called Interleukin 1 beta. This cytokine is also present in the skin and eye epithelial cells and is released when these cells are damaged by ultraviolet light.

Interleukin 1 beta then increases the excitability in the affected neurons, paving the way for HSV to explode, UVA researchers found.

“It is really remarkable that the virus has hijacked this pathway that is part of our body’s immune response,” said Cliffe. “It highlights how some viruses have evolved to take advantage of what should be part of our infection-fighting machine.”

The researchers say the discovery could lead to revolutionary new treatments in the field of virology, although more research needs to be done before this happens.

“A better understanding of what causes HSV to reactivate in response to a stimulus is needed to develop new therapies,” said Cliffe. “Ultimately, what we hope to do is target the latent virus itself and make it unresponsive to stimuli like Interleukin 1 beta.”

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