Investigation of the mechanisms by which antibody to VZV IE62 protein augments mechanical allodynia

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Acute herpetic pain and postherpetic neuralgia are intractable neurogenic pain, however the mechanisms of the pain are still unknown. We previously found that immunoreaction to antibody to IE62, one of immediate early protein produced by varicella zoster virus, augment mechanical allodynia in mice with peripheral nerve injury via activation of BDNF activity. In this research, we found that antibody to IE62 augment the acute herpetic pain and increase the transition to postherpetic neuralgia in mice. Using global gene expression analysis, we revealed that spinal galectin-3 is involved in the acute herpetic allodynia. However, we found that galectin-3 is not involved in the anti-IE62 antibody-mediated augmentation of mechanical allodynia.