In this study, we examined saliva for the presence of VZV DNA in immunocompetent individuals aged ≥60 years and grouped according to zoster status. Remarkably, we detected VZV DNA in saliva samples from subjects with a history of zoster up to 12 years after illness, regardless of whether they had PHN, whereas only 2 (12%) of 17 age-matched subjects with no zoster history showed VZV DNA in their samples. Note that neither the number of positive saliva samples nor the copy number of VZV DNA in saliva differed significantly between the subjects with zoster alone (group 1) and those with zoster and PHN (group 2), indicating that zoster predicts the presence of VZV DNA in saliva, not the chronic pain afterward. The detection of VZV DNA in the saliva of 2 subjects aged ≥60 years with no history of zoster is most likely the outcome of VZV reactivation without rash. This is not surprising given the magnitude of virologically confirmed VZV-induced neurological and ocular disease such as cerebellar ataxia, meningoencephalitis, VZV vasculopathy, myelitis, zoster sine herpete, and retinitis without any history of zoster rash (reviewed in [11
An earlier study reported the detection of VZV DNA in the saliva of 54 zoster patients examined, although the age range of those zoster patients was 21–82 years and their saliva was studied for only 3 weeks after zoster [9
]. The detection of VZV DNA [8
] and of infectious VZV [12
] in the saliva of healthy stressed astronauts points to the need to compare the duration of detectable VZV DNA in saliva of zoster patients <60 years old with that in zoster patients ≥60 years old. Furthermore, VZV DNA has also been detected in saliva of individuals ≥60 years old for 1 month after immunization with Zostavax (Zoster Vaccine Live) [13
], suggesting that human saliva should be examined for VZV DNA and infectious virus for longer times after immunization.
Although no immediate explanation is apparent for the persistence of VZV DNA in saliva of subjects with a history of zoster, our data support those of earlier studies which revealed that the presence of virus is not restricted to the affected dermatome. For example, VZV DNA was found in the saliva of each of 54 patients with zoster on the face, trunk, and upper and lower extremities [9
]. VZV DNA is also present in blood mononuclear cells during acute zoster [14
] as well as in blood mononuclear cells of some elderly individuals with no history of zoster [15
]. Overall, the detection of VZV DNA in saliva and blood indicates that after reactivation from ganglia, virus does more than travel transaxonally anterograde to skin. Furthermore, although the origin of VZV DNA in saliva is still unknown, infectious virus has been found in the saliva of patients with acute zoster [9
] and in healthy astronauts [12
]. The detection of VZV DNA in saliva of some elderly individuals for many years after zoster may reflect their inability to drive virus back to the latent state, just as a smoldering ganglionitis has been speculated to explain the development of postherpetic neuralgia [5
]. Both phenomena could readily be explained by individual differences in host-cell--mediated immune responses to VZV.
Finally, the potential usefulness of saliva in diagnosis of patients with neurological and ocular disease should be considered. Future studies are needed to establish whether VZV DNA can be detected in the saliva of such patients. To date, definitive virological confirmation has required blood and cerebrospinal fluid examination for VZV DNA and anti-VZV immunoglobulin G and M.