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Vaccination for the prevention of shingles (herpes zoster)

Author
Mary A Albrecht, MD
Section Editor
Martin S Hirsch, MD
Deputy Editor
Jennifer Mitty, MD, MPH

INTRODUCTION

Varicella-zoster virus (VZV) infection causes two clinically distinct forms of disease. Primary infection with VZV results in varicella, known as chickenpox, characterized by vesicular lesions in different stages of development on the face, trunk, and extremities. Herpes zoster, also known as shingles, results from reactivation of endogenous latent VZV infection within the sensory ganglia. This clinical form of the disease is characterized by a painful, unilateral vesicular eruption, which usually occurs in a restricted dermatomal distribution.

Vaccines are available for prevention of both infections. This topic will address the use of the live attenuated zoster vaccine (Zostavax) to prevent reactivation disease. A discussion of the vaccine used to prevent varicella (chickenpox) is found elsewhere. (See "Vaccination for the prevention chickenpox (primary varicella infection)".)

IMPORTANCE OF CELL-MEDIATED IMMUNITY

Varicella-zoster virus (VZV)-specific cell-mediated immune responses plays a critical role in controlling VZV latency and limiting the potential for reactivation [1-4]. A decline in cell-mediated VZV-specific immunity has been documented in older individuals and in patients with lymphoproliferative malignancies who experience higher rates of herpes zoster [3-5]. In contrast, children with hypogammaglobulinemia do not experience severely protracted or fulminant primary varicella infection, or increased rates of zoster [6]. These combined observations suggest that a decline in cell-mediated, rather than humoral, immunity is linked directly to reactivated VZV syndromes. These epidemiologic observations are supported by in vitro data that demonstrate reduced VZV T cell responder cell frequency in aging patients who are more susceptible to virus activation [7].

Immunity and risk of reactivation — A decline in cell-mediated immunity to varicella-zoster is regarded as the major precipitant for inducing VZV reactivation [3-5]. Approximately 30 to 40 percent of persons over the age of 55 years do not have any detectable VZV-specific T cell responses [8]. Zoster immunization is associated with a boost in VZV-specific T cell immune responses, which is the probable mechanism explaining the vaccine's efficacy in preventing or attenuating disease [9,10].

Among those who develop herpes zoster, in vitro data suggest that robust VZV cell-mediated immunity, at the onset of rash, is correlated with reduced severity of disease and less risk of postherpetic neuralgia [9]. Immunocompromised patients who lack adequate VZV-specific cellular immune responses are at greater risk for prolonged episodes of reactivation and disseminated disease, which can be fatal [8]. (See "Clinical manifestations of varicella-zoster virus infection: Herpes zoster".)

                          

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Literature review current through: Nov 2016. | This topic last updated: Fri Sep 23 00:00:00 GMT+00:00 2016.
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