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Review
. 2017 Jan;187(1):82-92.
doi: 10.1111/cei.12809. Epub 2016 Jul 25.

Herpes zoster and the search for an effective vaccine

Affiliations
Review

Herpes zoster and the search for an effective vaccine

N Arnold et al. Clin Exp Immunol. 2017 Jan.

Abstract

Primary infection with varicella zoster virus (VZV), an exclusively human neurotrophic alphaherpsesvirus, results in varicella, known more commonly as chickenpox. Like other alphaherpesviruses, VZV establishes latency in the sensory ganglia and can reactivate to cause herpes zoster (also known as shingles), a painful and debilitating disease, especially in elderly and immunocompromised individuals. The overall incidence of herpes zoster in Europe and the United States is three per 1000 people, but increases sharply after 60 years of age to 10 per 1000 people. Zostavax® is a vaccine approved by the Federal Drug Administration for the prevention of herpes zoster. Unfortunately, this vaccine reduces the incidence of disease by only 51% and the incidence of post-herpetic neuralgia by 66·5% when administered to those aged 60 and older. Moreover, it is contraindicated for individuals who are immunocompromised or receiving immunosuppressant treatments, although they are at higher risk for herpes zoster compared to immune-competent older individuals. This paper reviews VZV pathogenesis, host responses and current vaccines available to prevent herpes zoster.

Keywords: Zostavax®; herpesvirus; reactivation; shingles; vaccine.

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Figures

Figure 1
Figure 1
Varicella zoster virus (VZV) immune response during reactivation. When immune responses weaken, VZV reactivates by travelling anterograde towards nerve endings, replicates in keratinocytes and epithelial cells causing the formation of polykaryocytes, leading ultimately to a dermatomal rash. The local immune response in the ganglia is characterized by the infiltration of CD8, CD4, natural killer (NK) cells, macrophages and B cells. The immune response in the skin is characterized by CD4, CD8, NK cells and macrophages along with increased expression of interferon (IFN)‐γ, tumour necrosis factor (TNF)‐α and interleukin (IL)‐6.

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