Reply to Gilden et al

Abstract

TO THE EDITOR—Dr Gilden and his group have proposed that persistent or low-grade productive varicella-zoster virus (VZV) infection occurs in sensory ganglia of patients with postherpetic neuralgia (PHN) [1]. In Nagel’s excellent article [2], an observation that more VZV DNA was present in the saliva of patients with PHN than in saliva from patients without PHN would probably have been interpreted as consistent with this hypothesis, regardless of whether the immune system does or does not control VZV in PHN patients [3]. The fact that the incidence and concentration of prolonged shedding of VZV DNA in saliva was similar in both groups of patients, however, does not support the idea that prolonged replication of VZV causes PHN, although it does not rule it out. We do not know why VZV DNA is present in saliva of patients with herpes zoster and those postinfection [2, 4]. As Dr Gilden and his colleagues note, ganglionitis in PHN has not been directly associated with VZV, possibly, in part, because human ganglia are not readily available for study [1]. Because it is unclear whether the pathogenesis of zoster sine herpete is similar to that of PHN [1], responses to antiviral therapy may not be comparable in each of these conditions. Therefore, because zoster sine herpete responds to antiviral therapy, it does not necessarily follow that PHN will respond in a similar manner. I believe, however, that we can agree that the presence of VZV DNA in saliva and the etiology of PHN remain mysterious and deserve further study [1, 4].