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J Clin Virol. 2011 Feb;50(2):130-5. doi: 10.1016/j.jcv.2010.10.014. Epub 2010 Nov 18.

Persistence of varicella-zoster virus viraemia in patients with herpes zoster.

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Department of Infection, The Windeyer Institute, University College London, 46 Cleveland Street, London WC1T 4JF, England, UK.



Herpes zoster is caused by the reactivation of varicella-zoster virus from sensory neurons. The commonest complication following zoster is chronic pain termed post herpetic neuralgia.


To investigate the dynamics of VZV viraemia and viral load following the resolution of zoster and its relationship to PHN development.


Blood samples were collected at baseline, 1 month, 3 months and 6 month from a prospective study of 63 patients with active zoster. Quantification of VZV DNA in whole blood was performed using a real-time PCR assay.


During acute zoster, all patients had detectable VZV DNA in their blood. VZV DNA remained detectable in the blood of 91% of patients at 6 months although levels declined significantly (p<0.0001). A history of prodromal symptoms (p=0.005) and severity of pain at baseline (p=0.038) as well as taking antivirals (p=0.046) and being immunocompromised (p=0.043) were associated, with longer time to recovery from PHN. Viral DNA loads were consistently higher in patients with risk factors for PHN and higher viral DNA loads over time were associated with longer time to recovery (p=0.058 overall and 0.038 in immunocompetent).


Based on these observations we hypothesise that VZV replication persists following acute shingles and that higher viral DNA loads contribute to the risk factors for PHN.

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