The facial nerve consists of two roots: the motor division and the nervus intermedius, which contains parasympathetic fibers and sensory fibers. The cell bodies of the sensory fibers are in the geniculate ganglion, and some afferent fibers supply the mucous membranes of the oropharynx and the skin of the external auditory meatus and around the ear. VZV reactivation in the geniculate ganglia and subsequent inflammation of the facial nerve in the temporal bone are suspected to cause facial palsy (2
), while VZV migrates from the geniculate ganglia into the skin around the ear or into the oropharynx via the sensory fibers, where it replicates and produces zoster in RHS. In the present study, VZV DNA tended to be detectable in saliva from RHS patients who had zoster in the oropharyngeal epithelium, and the saliva from these patients contained a high copy number of the viral DNA. These results demonstrate the reliability of the TaqMan PCR assay because VZV replicates at the oropharyngeal lesions and is shed into the saliva. We have also shown that VZV DNA is detectable in saliva from patients with RHS who have zoster around the ear and from those with ZSH, suggesting that reactivated VZV in the geniculate ganglia may migrate into the oropharyngeal epithelium without producing zoster at the site.
Using the TaqMan PCR assay, the present study shows that the VZV copy number in saliva increases after the onset of facial palsy and peaks near the day of the appearance of zoster in RHS patients who exhibit facial palsy followed by zoster. In patients who exhibit zoster and facial palsy simultaneously, the VZV load gradually decreases after the onset or peaks several days later. Judging from these results, the viral load in saliva from patients with RHS may peak in accordance with the appearance of zoster. These results are consistent with those from a previous study that found a decrease in the amount of VZV DNA after the onset of varicella (10
). In patients who exhibit facial palsy several days after the appearance of zoster, viral replication may already have decreased at the onset of the palsy. Therefore, VZV DNA is less frequently detected in such patients. These findings suggest that the VZV load in saliva reflects the kinetics of viral reactivation.
Two patterns of the VZV load were also observed in PCR-positive patients with ZSH: a decrease after the first visit and a peak after it. These results indicate that the correlation between the kinetics of VZV reactivation and the onset of facial palsy in patients with ZSH is similar to that in patients with RHS. Based on the findings that VZV DNA is less frequently detected in RHS patients who exhibit facial palsy several days after the appearance of zoster, the VZV load may have decreased at the onset in some PCR-negative patients with ZSH.
We also found that the amounts of VZV DNA in saliva were not significantly different between RHS and ZSH. The data suggest that VZV reactivation in ZSH does occur at levels similar to those in RHS and that the VZV load does not play a major role in causing the different manifestations of RHS and ZSH. It has been reported that a VZV-specific T-cell response is correlated with the risk of herpes zoster (7
). In addition, depression of cellular immunity against VZV has been demonstrated in RHS and ZSH (9
). Therefore, different cellular immunoreactions to VZV at the mucocutaneous site may correlate with the appearance of zoster in facial palsy patients with VZV reactivation. Further studies on cellular immunity to VZV are needed to confirm this hypothesis.
Our results suggest the clinical utility of the TaqMan PCR assay for analysis of VZV replication during antiviral therapy. Acyclovir therapy has resulted in marked suppression of viremia in varicella (10
). In the present study, acyclovir reduced the VZV copy number in most cases of RHS and ZSH. These findings suggest that the TaqMan PCR assay may be useful in assessing the efficacy of acyclovir therapy.
In conclusion, the present study shows that the VZV load in saliva reflects the kinetics of viral reactivation in patients with RHS and ZSH. In addition, our findings suggest that the VZV load is not the major cause of differences between RHS and ZSH.