Effect of Viral Load on the outcome of Herpes Zoster

Centre for Infectious Disease, Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, Queen Mary College, 4 Newark St, London E1 2AT, England, UK.; Section of Applied Statistics, School of Biological Sciences, University of Reading, P. O. Box 240, Earley Gate, Reading RG6 6FN, England, UK.; Centre for Haematology, Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, Queen Mary College, 4 Newark St, London E1 2AT, England, UK.; Pain Management Clinic, Level 4, Bristol Royal Infirmary, Bristol BS2 8HW, UK

^* To whom correspondence should be addressed. Email: j.breuer{at}qmul.ac.uk.

	Abstract

VZV is a member of the Herpesviridae family, primary infection with which causes varicella, more commonly known as chicken pox. Characteristic of members of the alpha herpes virus sub-family, VZV is neurotropic and establishes latency in sensory neurons. Reactivation of VZV causes herpes-zoster, also known as shingles. The most frequent complication following zoster is chronic and often debilitating pain called PHN, which can last for months after the disappearance of rash. During episodes of acute zoster, VZV viraemia occurs in some but not all patients, however, the effect of viral load on disease outcome is not known. Here we describe the development of a highly specific, sensitive and reproducible real-time PCR assay to investigate the factors that may contribute to the presence and levels of baseline viraemia in patients with zoster and to determine the relationship between viraemia and the development and persistence of PHN. VZV DNA was detected in PBMCs of 78% of patients with acute zoster and in 9% of healthy asymptomatic blood donors. Presence of VZV in PBMCs of patients with acute zoster was independently associated with age and being on antivirals but not with gender, immune status, extent of rash, age of rash at time of blood sampling, having a history of prodromal pain, or the extent of acute pain. Prodromal pain was significantly associated with higher baseline viral loads. Viral load levels were not associated with the development or persistence of PHN at 6, 12, or 26 weeks.