The results of a study by researchers at the University of Colorado Anschutz suggest that extracellular vesicles known as exosomes in the blood are the likely culprit behind why some people with shingles experience lingering pain—post-herpetic neuralgia (PHN)—long after the causative varicella zoster virus (VZV) has cleared the body.
Exosomes are microscopic packages released by cells that carry proteins and other molecules throughout the body. The research team found that a shingles infection can cause nerve cells to release inflammatory signals and become highly active. When investigators exposed healthy nerve cells in the lab to exosomes collected from the blood of people with PHN, they found that the exosomes triggered in the nerve cells many of the same harmful changes seen during viral infection, even though no virus was present.
The findings suggest that PHN may develop because the body fails to fully turn off the healing response after shingles. Even after the virus has been cleared, exosomes continue delivering damaging messages that prevent nerves from recovering normally. The study results indicate that chronic shingles pain may not simply be the result of damage caused during the initial infection, but rather that biological signals carried by exosomes may keep nerve cells in an irritated, dysfunctional state. This opens the door to new approaches for predicting, preventing, and treating post-herpetic neuralgia.
The researchers, led by Andrew Bubak, PhD, reported their findings in Annals of Neurology, concluding that persistent exosome-mediated signaling sustains maladaptive neuronal remodeling after viral clearance, identifying circulating exosome cargo as potential therapeutic targets. This research underscores the need for a deeper understanding of the mechanisms driving the transition from acute viral injury to chronic pain, which may lead to innovative treatment strategies.
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