Decreased Immunity to Varicella Zoster Virus in Giant Cell Arteritis.

Christien Rondaan,Nicolaas A Bos,Annemieke M H Boots,Kornelis S M Van Der Geest,Elisabeth Brouwer,Johanna Westra,Elisabeth Eelsing

doi:10.3389/fimmu.2017.01377

Christien Rondaan, Nicolaas A Bos + Show 5 more

Open Access

https://doi.org/10.3389/fimmu.2017.01377

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Abstract

Herpes zoster, which can have a major impact on quality of life, results from reactivation of a latent varicella zoster virus (VZV) infection. We hypothesized that giant cell arteritis (GCA) patients are at increased risk of herpes zoster because of treatment with high-dose glucocorticoids and advanced age. Aim of the study, therefore, was to determine cell-mediated and humoral immunity to VZV in patients with GCA, patients with closely related disease polymyalgia rheumatica (PMR; treated with lower doses of glucocorticoids) and healthy controls (HCs). Cell-mediated immunity to VZV was determined by performing interferon-γ (IFNγ) enzyme-linked immunospot and intracellular cytokine flow cytometry measurements in 11 GCA and 15 PMR patients and in 26 age/sex-matched HCs. Immunoglobulin G antibodies to VZV glycoprotein (VZV-IgG) were measured in serum samples of 35 GCA and 26 PMR patients at different times of follow-up and in 58 age and sex-matched HCs by an enzyme-linked immunosorbent assay. The number of VZV-specific IFNγ spot-forming cells was significantly lower in GCA patients on treatment, than in age-matched HCs (p = 0.029), but was not different in PMR patients on treatment. Similar levels of VZV-IgG were found in GCA and PMR patients at baseline, compared to HCs. The finding of a decreased cell-mediated immunity to VZV, known to be of great importance in defense to the virus, indicates an increased herpes zoster risk in GCA patients compared to an already at-risk elderly population. Herpes zoster vaccination is, therefore, of special importance in GCA patients, and would ideally be administered at time of diagnosis. Interestingly, as VZV was suggested to be the trigger in GCA pathogenesis, similar levels of VZV-IgG were found in GCA patients at time of diagnosis and age-matched HCs, indicating that GCA patients did not experience herpes zoster substantially more often in the months preceding diagnosis than controls.

Highlights

Herpes zoster is caused by reactivation of a latent varicella zoster virus (VZV) infection [1]
Serum was stored at −20°C, and peripheral blood mononuclear cell (PBMC) were stored in liquid nitrogen until use
After evaluating cell viability by trypan blue staining, PBMCs were used in enzyme-linked immunospot (ELISpot) assays and flow cytometry analyses

Summary

Introduction

Herpes zoster is caused by reactivation of a latent varicella zoster virus (VZV) infection [1]. Almost the whole adult population of temperate countries has experienced a primary VZV infection in childhood (known as varicella or chickenpox) and is, at risk of herpes zoster [2]. Postherpetic neuralgia (pain lasting >90 days after onset of rash) is the most common complication of herpes zoster occuring in 8–27% of patients [3,4,5,6]. Impact on quality of life of herpes zoster and postherpetic neuralgia can be major [3, 4]. A rise in the incidence of herpes zoster occurs concomitantly with a decline in VZV-specific cell-mediated immunity. The estimated incidence of HZ is about 3.4–4.82 per 1,000 person years in the general population which increases to more than 11 per 1,000 person years in those above 80 years of age [7]

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