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. 2021 Sep 30;224(12 Suppl 2):S429-S442.
doi: 10.1093/infdis/jiab387.

Herpes Zoster Vaccines

Ruth Harbecke  1   2 , Jeffrey I Cohen  3 , Michael N Oxman  1   2   4
Affiliations

Herpes Zoster Vaccines

Ruth Harbecke et al. J Infect Dis. .

Abstract

Herpes zoster (HZ) affects approximately 1 in 3 persons in their lifetime, and the risk of HZ increases with increasing age. The most common, debilitating complication of HZ is the chronic neuropathic pain of postherpetic neuralgia (PHN). Two herpes zoster vaccines, a live-attenuated varicella-zoster virus (VZV) vaccine (zoster vaccine live [ZVL]; ZOSTAVAX [Merck]) and an adjuvanted VZV glycoprotein E (gE) subunit vaccine (recombinant zoster vaccine [RZV]; SHINGRIX [GlaxoSmithKline]) are licensed for the prevention of HZ and PHN in healthy older adults. The safety and efficacy of both vaccines has been demonstrated in clinical trials in immunocompetent adults and in selected immunocompromised persons and persons with immune-mediated diseases. Numerous real-world effectiveness studies have confirmed the safety and effectiveness of both ZVL and RZV. Recombinant zoster vaccine (RZV) is more effective for prevention of HZ than ZVL. Recombinant zoster vaccine is nonreplicating and is thus safe in immunocompromised persons. Additional zoster vaccines are in different stages of development. Wider distribution of safe and effective zoster vaccines will improve the health and well being of the rapidly growing population of older adults around the world.

Keywords: herpes zoster; live attenuated Oka varicella-zoster vaccine; recombinant zoster vaccine; zoster vaccine.

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Figures

Figure 1.
Figure 1.
Classical herpes zoster in the left T4 dermatome. Note the concentration of lesions in areas of the dermatome innervated by the posterior primary division and the lateral branch of the anterior primary division of the left T4 spinal nerve. Source: Levin et al [2].
Figure 2.
Figure 2.
During varicella, varicella-zoster virus (VZV) establishes life-long latency in neurons in sensory ganglia. Herpes zoster results when latent virus reactivates, multiplies in the ganglion, and spreads back down the sensory nerve. Varicella induces immunity to VZV that prevents reactivating virus from multiplying, thus preventing herpes zoster. This immunity decreases over time until it falls below a critical threshold, permitting reactivating VZV to multiply and cause herpes zoster. The age-related decline in VZV-specific immunity is slowed by periodic stimulation due to exogenous exposure to VZV from contact with varicella and by episodes of reactivation of latent VZV where host immunity inhibits virus multiplication before it can cause herpes zoster (contained reversions). Modified from R Edgar Hope-Simpson [15].
See this image and copyright information in PMC

References

    1. The complete reference list is available as supplementary material.
    1. Hope-Simpson RE. The nature of herpes zoster: a long-term study and a new hypothesis. Proc R Soc Med 1965; 58:9–20. - PMC - PubMed
    1. Oxman MN. Zoster vaccine: current status and future prospects. Clin Infect Dis 2010; 51:197–213. - PubMed
    1. Oxman MN. Clinical manifestations of herpes zoster. In: Arvin AM, Gershon AA, eds. Varicella-Zoster Virus: Virology and Clinical Management. Cambridge, UK: Cambridge University Press, 2000:246–75.
    1. Harpaz R, Leung JW. The epidemiology of herpes zoster in the United States during the era of varicella and herpes zoster vaccines: changing patterns among older adults. Clin Infect Dis 2019; 69:341–4. - PubMed

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