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. 2001 Aug;39(8):2856-9.
doi: 10.1128/JCM.39.8.2856-2859.2001.

Quantitation of varicella-zoster virus DNA in patients with Ramsay Hunt syndrome and zoster sine herpete

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Quantitation of varicella-zoster virus DNA in patients with Ramsay Hunt syndrome and zoster sine herpete

Y Furuta et al. J Clin Microbiol. 2001 Aug.

Abstract

Varicella-zoster virus (VZV) reactivation causes facial nerve palsy in Ramsay Hunt syndrome (RHS) and zoster sine herpete (ZSH) with and without zoster rash, respectively. In the present study, we analyzed the VZV DNA copy number in saliva samples from 25 patients with RHS and 31 patients with ZSH using a TaqMan PCR assay to determine differences in the viral load between the two diseases. VZV copy number in saliva peaked near the day of the appearance of zoster in patients with RHS. Consequently, VZV DNA was less frequently detected in patients with RHS who exhibited facial palsy several days after the appearance of zoster. These findings suggest that the VZV load in saliva samples reflects the kinetics of viral reactivation in patients with RHS. In addition, VZV DNA was equally detected in saliva from patients with RHS and ZSH, and there was no significant difference in the highest viral copy number between patients with RHS and those with ZSH. The VZV load does not appear to reflect a major difference between RHS and ZSH.

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Figures

FIG. 1
FIG. 1
Transition of VZV DNA load in patients with RHS and ZSH. ●, VZV DNA copies, expressed as the copy number/50 μl of saliva (logarithmic scales). Dotted lines indicate the minimum detection level of VZV DNA. (A) Patient with RHS in whom zoster and facial palsy appeared simultaneously (day 0). This patient was treated with acyclovir by infusion at 750 mg per day for 7 days. The VZV DNA levels gradually decreased and became undetectable on day 8. (B) Patient with RHS who exhibited zoster 6 days after the onset of facial palsy. Acyclovir treatment (4,000 mg in tablets daily for 7 days) started on day 5 before the appearance of zoster because VZV DNA was detected in saliva obtained on day 4. The VZV DNA levels peaked 1 day before the appearance of skin lesions. (C) A patient with ZSH treated with acyclovir by infusion at 750 mg per day for 5 days. The VZV copy number gradually decreased and became undetectable on day 6. (D) A patient with ZSH who did not receive antiviral therapy. The VZV copy number peaked on day 5.
FIG. 2
FIG. 2
Quantitation of VZV DNA in saliva samples from patients with RHS and ZSH. The highest copy number in each patient was plotted (logarithmic scales). Samples below the dotted line were negative for VZV DNA. Open circles indicate patients who had zoster in the oropharyngeal epithelium. N.S., not significant.

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