Neuropathic pain resulting from nerve injury is a serious clinical problem. Currently, there is no effective therapy for the treatment. Among all choices, herpes simplex virus (HSV)-based vectors offers a unique advantage over other therapies because HSV-based vectors can achieve a local delivery of transgenes in the peripheral nerve system thus avoiding the side effects associated with systemic administration of therapeutic compounds or peptides. HSV-based therapies hold promise in the treatment of neuropathic pain but continuous expression of transgenes might produce unwanted effects locally, thus it will be desirable to develop regulatable therapies for the treatment.
Our current work work is focused on elucidating the role of the chemokine fractalkine in the pathogenesis of neuropathic pain and developing a HSV based soluble fractalkine receptor expressing vector for the treatment in a rat model of chronic compression injury.