A breakthrough discovery on the causes of herpes flareups by researchers at the University of Virginia School of Medicine may provide new ways to prevent cold sores and recurrent herpes related eye disease.
The study, published on Wednesday in the scientific journal eLife, seems to have discovered the operating mechanism which causes things like stress, fever and sunburn to activate herpes flareups.
“Herpes simplex recurrence has long been associated with stress, fever and sunburn,” said researcher Anna R. Cliffe, PhD, of UVA’s Department of Microbiology, Immunology and Cancer Biology. “This study sheds light on how all these triggers can lead to herpes simplex-associated disease.”
Herpes simplex virus-1 (HSV-1) is one of the most common human pathogens in existence, present in approximately 40–90% of the population worldwide, producing a latent infection in neurons, which is reactivated every so often for the rest of the infected individual’s lifetime.
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 severe eye disease which, 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 her collaborators found that when HSV-infected neurons were exposed to stimuli that induce “neuronal hyperexcitation,” the virus was able to sense the particular change and seize on the opportunity to reactivate.
Working in a model developed by the Cliffe lab which looks at HSV-infected neurons 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 particular cytokine called Interleukin 1 beta. This cytokine is also present in epithelial cells in the skin and eye and is released when these cells are damaged by ultraviolet light.
Interleukin 1 beta then increases the excitability in the affected neurons, setting the stage for HSV to flare up, the UVA researchers discovered.
“It is really remarkable that the virus has hijacked this pathway that is part of our body’s immune response,” Cliffe said. “It highlights how some viruses have evolved to take advantage of what should be part of our infection-fighting machinery.”
The researchers claim the discovery could lead to revolutionary new treatments in the field of virology, though more research would need to be done before that could happen.
“A better understanding of what causes HSV to reactivate in response to a stimulus is needed to develop novel therapeutics,” Cliffe said. “Ultimately, what we hope to do is target the latent virus itself and make it unresponsive to stimuli such as Interleukin 1 beta.”