Korean J Pain.  2013 Jul;26(3):242-248. 10.3344/kjp.2013.26.3.242.

Herpes Zoster Vaccination

• Kim KH

• KMID: 2074024
• DOI: http://doi.org/10.3344/kjp.2013.26.3.242

Abstract

Varicella (chickenpox) is a highly contagious airborne disease caused by primary infection with the varicella zoster virus (VZV). Following the resolution of chickenpox, the virus can remain dormant in the dorsal sensory and cranial ganglion for decades. Shingles (herpes zoster [HZ]) is a neurocutaneous disease caused by reactivation of latent VZV and may progress to postherpetic neuralgia (PHN), which is characterized by dermatomal pain persisting for more than 120 days after the onset of HZ rash, or "well-established PHN", which persist for more than 180 days. Vaccination with an attenuated form of VZV activates specific T-cell production, thereby avoiding viral reactivation and development of HZ. It has been demonstrated to reduce the occurrence by approximately 50-70%, the duration of pain of HZ, and the frequency of subsequent PHN in individuals aged > or = 50 years in clinical studies. However, it has not proved efficacious in preventing repeat episodes of HZ and reducing the severity of PHN, nor has its long-term efficacy been demonstrated. The most frequent adverse reactions reported for HZ vaccination were injection site pain and/or swelling and headache. In addition, it should not be administrated to children, pregnant women, and immunocompromised persons or those allergic to neomycin or any component of the vaccine.

Keyword

chickenpox; herpes zoster; herpes zoster vaccine; human herpesvirus 3; postherpetic neuralgia

MeSH Terms

Aged
Chickenpox
Child
Exanthema
Female
Ganglion Cysts
Headache
Herpes Zoster
Herpes Zoster Vaccine
Herpesvirus 3, Human
Humans
Neomycin
Neuralgia, Postherpetic
Pregnant Women
T-Lymphocytes
Vaccination
Viruses
Herpes Zoster Vaccine
Neomycin

Figure

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  Fig. 1 The pathogenesis of varicella, herpes zoster, and postherpetic neuralgia. (A) Varicella zoster virus (VZV) structure and taxonomy. (B) Varicella (chickenpox) pathogenesis-infection of VZV is initiated through inhalation and exposure of the mucous membranes of the respiratory tract to the virus. Initially, replication occurs in the regional lymph nodes followed by cell-associated viraemia during which the virus infects peripheral blood monocyte cells (PBMCs). Progeny virus is then disseminated to reticuloendothelial cells in the liver, spleen, and other organs. Virion release from reticuloendothelial cells initiates by a second phase of cell-associated viraemia, spreading VZV to the skin. During the resolution of varicella, VZV establishes latency in the trigeminal and dorsal root ganglia. VZV exhibits multiple cell tropisms (), infecting PBMCs and skin cells before establishing latency in the sensory neurons. (C) Herpes zoster (HZ) and postherpetic neuralgia (PHN) pathogenesis-VZV reactivation initiates the development of HZ. Reactivated VZV multiplies and spreads within the ganglion, causing neuronal necrosis, intense inflammation, and a process that often results in severe neuralgia. VZV then spreads outwardly down sensory nerves causing intense neuritis. Virus progeny are then released from sensory nerve endings in the skin producing characteristic clusters of zoster vesicles. HZ and PHN pathogenesis can be divided into 3 phases: acute herpetic neuralgia, subacute herpetic neuralgia, and postherpetic neuralgia.

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  Fig. 2 Future outcome studies on varicella and herpes zoster (HZ) vaccination are needed. The first varicella vaccine recipients were 12 months old in 1995 and recently reached the age of 19 years. Information regarding an increased incidence of HZ due to reactivation of latent VZV will be available when these individuals reach 50 and 80 years of age in 2044 and 2074, respectively. HZ vaccination began in 2006 and 2011 in individuals aged ≥ 60 and ≥ 50 years, respectively. Long-term efficacy can be evaluated when these individuals reach the age of 80 years in 2026 and 2041, respectively.

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