The incidence and clinical characteristics of herpes zoster among children and adolescents after implementation of varicella vaccination.
ABSTRACT The varicella-zoster virus (VZV) vaccine strain may reactivate to cause herpes zoster. Limited data suggest that the risk of herpes zoster in vaccinated children could be lower than in children with naturally acquired varicella. We examine incidence trends, risk and epidemiologic and clinical features of herpes zoster disease among children and adolescents by vaccination status.
Population-based active surveillance was conducted among <20 years old residents in Antelope Valley, California, from 2000 through 2006. Structured telephone interviews collected demographic, varicella vaccination and disease histories, and clinical information.
From 2000 to 2006, the incidence of herpes zoster among children<10 years of age declined by 55%, from 42 cases reported in 2000 (74.8/100,000 persons; 95% confidence interval [95% CI]: 55.3-101.2) to 18 reported in 2006 (33.3/100,000; 95% CI: 20.9-52.8; P<0.001). During the same period, the incidence of herpes zoster among 10- to 19-year-olds increased by 63%, from 35 cases reported in 2000 (59.5/100,000 persons; 95% CI: 42.7-82.9) to 64 reported in 2006 (96.7/100,000; 95% CI: 75.7-123.6; P<0.02). Among children aged<10 years, those with a history of varicella vaccination had a 4 to 12 times lower risk for developing herpes zoster compared with children with history of varicella disease.
Varicella vaccine substantially decreases the risk of herpes zoster among vaccinated children and its widespread use will likely reduce overall herpes zoster burden in the United States. The increase in herpes zoster incidence among 10- to 19-year-olds could not be confidently explained and needs to be confirmed from other data sources.
- [Show abstract] [Hide abstract]
ABSTRACT: Varicella is a highly contagious disease caused by primary infection with varicella zoster virus (VZV). VZV infection, as well as varicella vaccination, induces VZV-specific antibody and T-cell-mediated immunity, essential for recovery. The immune responses developed contribute to protection following re-exposure to VZV. When cell-mediated immunity declines, as occurs with aging or immunosuppression, reactivation of VZV leads to herpes zoster (HZ). It has been almost 20 years since universal varicella vaccination has been implemented in many areas around the globe and this has resulted in a significant reduction of varicella-associated disease burden. Successes are reviewed here, whilst emphasis is put on the challenges ahead. Most countries that have not implemented routine childhood varicella vaccination have chosen to vaccinate high-risk groups alone. The main reasons for not introducing universal vaccination are discussed, including fear of age shift of peak incidence age and of HZ incidence increase. Possible reasons for not observing the predicted increase in HZ incidence are explored. The advantages and disadvantages of universal vs targeted vaccination as well as different vaccination schedules are discussed.Therapeutic advances in vaccines. 03/2014; 2(2):39-55.
- [Show abstract] [Hide abstract]
ABSTRACT: 1083 ESPID REPoRtS anD REvIEwS T he live-attenuated vaccine has been the object of many recent reviews 1,2 ; there-fore, the focus here is an attempt to recon-sider whether this vaccine is the optimal means of preventing the disease complex of varicella-zoster virus (VZV) infection. In addressing this question, it will review the accrued knowledge of strategies in vaccine development, and how these vary depending on the nature of the infection to be prevented, along with technical advances in vaccine pro-duction that potentially allow us to achieve the goal of prevention of varicella infection, as opposed to reduction of disease symptoms. The majority of infectious diseases prevented by immunization have only an acute phase and therefore to be successful such a vaccine needs only to prevent disease. A common feature to these vaccines is that they do not prevent infection—exposure or a subclinical infection in the form of natural booster may even constitute a benefit—but they generally efficiently prevent disease. Some diseases have both an acute and a chronic phase: vaccines against such diseases are generally considered to be more difficult to develop because to fulfill both roles these vaccines need to prevent infection. The vaccines against hepatitis B (HBV) and human papilloma virus (HPV) infection are the proof-of-concept that vac-cines can prevent infection. The vaccine against HBV has accomplished its primary aim, that is, to prevent HBV infection in infancy and young children that leads in a vast majority of cases to a chronic infection and later in life to cirrhosis and cancer. The vaccine against HPV infection has not yet been shown to prevent cancer, but because it prevents the persistent infection that the immune system is unable to clear it is reason-able to assume that it will prevent the ensuing cancer development. The active component of both vaccines is virus-like particles, which represent empty, nonreplicating, particles expressing major viral surface protein(s), suggesting this is at least one route to creat-ing successful vaccines against chronic viral infections. Live vaccines against diseases with a chronic phase are more problematic. The Bacillus Calmette-Guérin vaccine will pre-vent acute disease(s) when given to infants but will not prevent infection (latent tubercu-losis) or will do so for a very short period of time. However, the Bacillus Calmette-Guérin vaccine does not seem to have the additional problem of a live vaccine against a disease with a chronic phase, that is, to cause latent infection by itself. This may be either because of the intradermal route of admin-istration or the attenuated strain not being based on Mycobacterium tuberculosis but on Mycobacterium bovis, a bacterium known to be able to cause acute disease but not latent infection in humans. The live vaccine against varicella on the other hand presents both shortcomings of not preventing latent infec-tion and of causing latent infection. The vaccine against varicella is the same kind of live-attenuated vaccine as those against measles, mumps and rubella. These vaccines consist of clinical isolates that have been attenuated by serial in vitro pas-sages with the aim to induce a genetically stable virus that no longer causes clinically significant disease but will induce immunity. The amount of virus in these live vaccines is very small, in the thousands or ten thousands, compared with the many millions of virus particles in inactivated viral vaccines so the multiplication of the virus will occur during the asymptomatic systemic infection. Based on the mechanism of action of live vaccines and the nature of VZV infec-tion, it is to be expected that the varicella vac-cine will also invariably give rise to latency. 3,4 The Japanese pioneers in the field have in recent years advanced the hypothesis 5 that the vaccine would not infect every child but only those who develop a rash after vaccina-tion. The hypothesis is neither supported by mechanistic considerations nor by a follow-up study by the Center for Disease Control in the United States, which stated 6 "it should be noted that herpes zoster has also been reported in vaccine recipients in whom no previous vaccine-related varicella-like rash was identified."The Pediatric Infectious Disease Journal 10/2014; 33(10):1083. · 3.14 Impact Factor
- [Show abstract] [Hide abstract]
ABSTRACT: The objective of this study was to characterise the incidence rates of herpes zoster (HZ), also known as shingles, and risk of complications across the world.BMJ Open 06/2014; 4(6):e004833. · 2.06 Impact Factor