IL-1β involved in triggering herpes simplex flares
Researchers have identified interleukin-1β (IL-1β) as a triggering factor for flares of herpes simplex virus (HSV) and the formation of cold sores.
In a press release from the University of Virginia (UVA) School of Medicine, the research team described how they sought to identify a common factor between known promoters of HSV flares, such as stress, illness and sunburn.
“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.”
In the paper published in eLife (Dec. 20, 2020; 9:e58037), the authors describe that when mouse model neurons harbouring the virus were exposed to stimuli that induce ‘neuronal hyperexcitation,’ the result was a reactivation of the virus.
In the press release, they note that during prolonged periods of inflammation or stress in humans, the immune system releases IL-1β. They add that IL-1β is also present in epithelial cells in the skin and eye and is released when these cells become damaged by ultraviolet light.
In turn, IL-1β increases the excitability of neurons, setting the stage for HSV to flare.
“It is really remarkable that the virus has hijacked this pathway that is part of our body’s immune response,” Dr. Cliffe said. “It highlights how some viruses have evolved to take advantage of what should be part of our infection-fighting machinery.”
In the release, the investigators said more research will need to be performed to fully understand the potential factors that play into herpes simplex disease. These factors include viral strains or types of neurons infected. Another outstanding question, they say, is whether HSV alters how neurons respond to cytokines such as IL-1β.
However, this new information adds to the understanding of the interactions between neurons and the immune system in herpes simplex, which could lead to new approaches to preventing flares.
“A better understanding of what causes HSV to reactivate in response to a stimulus is needed to develop novel therapeutics,” Dr. Cliffe said. “Ultimately, what we hope to do is target the latent virus itself and make it unresponsive to stimuli such as [IL-1β].”