Plerixafor may treat intractable post-herpetic neuralgia

Abstract

Varicella-zoster virus (VZV) causes varicella (chicken pox) and establishes latency in ganglia. A reactivation of latent VZV leads to herpes zoster (shingles). Herpes zoster often causes herpetic pain that can last for months or years after the rash has healed. Prolonged herpetic pain is defined as post-herpetic neuralgia (PHN). There is an unmet need to explore novel therapeutic approaches for intractable PHN. Postmortem studies have shown that VZV induces neuro-inflammation and damage to the ganglia and spinal cord. These pathological changes may be critical factors resulting in PHN. Accumulated evidence suggests that stem cells may alleviate neuropathic pain in animal models through immunomodulatory actions and neuronal repair. Unfortunately, exogenous stem cell transplantation has limited clinical use due to safety concerns, immune rejection, and complications. Pharmacological mobilization of endogenous bone marrow stem cells may overcome these obstacles. Plerixafor is a SDF-1/CXCR4 axis blocker which can stimulate the release of stem cells from the bone marrow into blood circulation. We propose a hypothesis that endogenous stem cells mobilized by plerixafor may relieve the symptoms of PHN. If so, it may represent a novel approach for the treatment of intractable PHN.