Context
Although the underlying cause of rheumatoid arthritis (RA) has not been determined, studies in animal models have identified several contributing factors. Notably, it has been observed that numerous physiological changes occur in both the peripheral and central nervous system during the onset of disease. Among these are the spinal and supraspinal release of endogenous opioids, such as met-enkephalin (ME). These peptides have been shown to be involved in the control of pain and can inhibit inflammatory processes. In previous work, it has been shown that following infection of sensory neurons with recombinant herpes simplex virus (HSV), the virus undergoes retrograde transport to the nucleus of the neuron in the dorsal root ganglion (DRG). Following infection of the footpad of rats with recombinant HSV containing the ME coding region, ME expression was detected in the DRG and in the peripheral fibers. In this study, the authors wanted to determine if overproduction of ME in the sensory neurons of rats could block pathologies of adjuvant-induced arthritis.