HSV delivery of a ligand-regulated endogenous ion channel gene to sensory neurons results in pain control following channel activation

Citation for published article

Goss, J. R., Cascio, M., Goins, W. F., Huang, S., Krisky, D. M., Clarke, R. J., Johnson, J. W., Yokoyama, H., Yoshimura, N., Gold, M. S., & Glorioso, J. C. (2011). HSV Delivery of a Ligand-regulated Endogenous Ion Channel Gene to Sensory Neurons Results in Pain Control Following Channel Activation. Molecular Therapy, 19(3), 500–506. https://doi.org/10.1038/mt.2010.246



Peer Reviewed


Document Type

Journal Article


Bayer School of Natural and Environmental Sciences

Primary Author Department

Chemistry and Biochemistry


Persistent pain remains a tremendous health problem due to both its prevalence and dearth of effective therapeutic interventions. To maximize pain relief while minimizing side effects, current gene therapy-based approaches have mostly exploited the expression of pain inhibitory products or interfered with pronociceptive ion channels. These methods do not enable control over the timing or duration of analgesia, nor titration to analgesic efficacy. Here, we describe a gene therapy strategy that potentially overcomes these limitations by providing exquisite control over therapy with efficacy in clinically relevant models of inflammatory pain. We utilize a herpes simplex viral (HSV) vector (vHGlyRα1) to express a ligand-regulated chloride ion channel, the glycine receptor (GlyR) in targeted sensory afferents; the subsequent exogenous addition of glycine provides the means for temporal and spatial control of afferent activity, and therefore pain. Use of an endogenous inhibitory receptor not normally present on sensory neurons both minimizes immunogenicity and maximizes therapeutic selectivity. © The American Society of Gene & Cell Therapy.