DNA MAPPING OF PAIRED VARICELLA-ZOSTER VIRUS ISOLATES FROM PATIENTS WITH SHINGLES
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Varicella–zoster virus is the cause of both varicella (chickenpox) and herpes zoster (shingles). A live attenuated varicella vaccine was developed in Japan in 1974, and in 1995 it was approved for use in the United States. The policy of universal vaccination of susceptible children and adults has had a profound effect on the epidemiology of varicella. Its effect on the epidemiology of zoster remains to be seen, in part because of the long delay between primary infection with varicella–zoster virus and the subsequent occurrence of zoster.Before varicella vaccine was introduced, chickenpox developed in approximately 4 million persons, most of . . .
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Background: Biological interactions between varicella (chickenpox) and herpes zoster (shingles), two diseases caused by the varicella zoster virus (VZV), continue to be debated including the potential effect on shingles cases following the introduction of universal childhood chickenpox vaccination programs. We investigated how chickenpox vaccination in Alberta impacts the incidence and age-distribution of shingles over 75 years post-vaccination, taking into consideration a variety of plausible theories of waning and boosting of immunity.Methods: We developed an agent-based model representing VZV disease, transmission, vaccination states and coverage, waning and boosting of immunity in a stylized geographic area, utilizing a distance-based network. We derived parameters from literature, including modeling, epidemiological, and immunology studies. We calibrated our model to the age-specific incidence of shingles and chickenpox prior to vaccination to derive optimal combinations of duration of boosting (DoB) and waning of immunity. We conducted paired simulations with and without implementing chickenpox vaccination. We computed the count and cumulative incidence rate of shingles cases at 10, 25, 50, and 75 years intervals, following introduction of vaccination, and compared the difference between runs with vaccination and without vaccination using the Mann-Whitney U-test to determine statistical significance. We carried out sensitivity analyses by increasing and lowering vaccination coverage and removing biological effect of boosting.Results: Chickenpox vaccination led to a decrease in chickenpox cases. The cumulative incidence of chickenpox had dropped from 1,254 cases per 100,000 person-years pre chickenpox vaccination to 193 cases per 100,000 person-years 10 years after the vaccine implementation. We observed an increase in the all-ages shingles cumulative incidence at 10 and 25 years post chickenpox vaccination and mixed cumulative incidence change at 50 and 75 years post-vaccination. The magnitude of change was sensitive to DoB and ranged from an increase of 22-100 per 100,000 person-years at 10 years post-vaccination for two and seven years of boosting respectively (p < 0.001). At 75 years post-vaccination, cumulative incidence ranged from a decline of 70 to an increase of 71 per 100,000 person-years for two and seven years of boosting respectively (p < 0.001). Sensitivity analyses had a minimal impact on our inferences except for removing the effect of boosting.Discussion: Our model demonstrates that over the longer time period, there will be a reduction in shingles incidence driven by the depletion of the source of shingles reactivation; however in the short to medium term some age cohorts may experience an increase in shingles incidence. Our model offers a platform to further explore the relationship between chickenpox and shingles, including analyzing the impact of different chickenpox vaccination schedules and cost-effectiveness studies. PMID: 29942688
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Varicella zoster virus (VZV) is one of the eight known human herpesviruses. Initial VZV infection results in chickenpox, while viral reactivation following a period of latency manifests as shingles. Separate vaccines exist to protect against both initial infection and subsequent reactivation. Controversy regarding chickenpox vaccination is contentious with most countries not including the vaccine in their childhood immunization schedule due to the hypothesized negative impact on immune-boosting, where VZV reactivation is suppressed through exogenous boosting of VZV antibodies from exposure to natural chickenpox infections.Population-level chickenpox and shingles notifications from Thailand, a country that does not vaccinate against either disease, were previously fitted with mathematical models to estimate rates of VZV transmission and reactivation. Here, multiple chickenpox and shingles vaccination scenarios were simulated and compared to a model lacking any vaccination to analyze the long-term impacts of VZV vaccination.As expected, simulations suggested that an introduction of the chickenpox vaccine, at any coverage level, would reduce chickenpox incidence. However, chickenpox vaccine coverage levels above 35% would increase shingles incidence under realistic estimates of shingles coverage with the current length of protective immunity from the vaccine. A trade-off between chickenpox and shingles vaccination coverage was discovered, where mid-level chickenpox coverage levels were identified as the optimal target to minimize total zoster burden. Only in scenarios where shingles vaccine provided lifelong immunity or coverage exceeded current levels could large reductions in both chickenpox and shingles be achieved.The complicated nature of VZV makes it impossible to select a single vaccination scenario as universal policy. Strategies focused on reducing both chickenpox and shingles incidence, but prioritizing the latter should maximize efforts towards shingles vaccination, while slowly incorporating chickenpox vaccination. Alternatively, countries may wish to minimize VZV complications of both chickenpox and shingles, which would lead to maximizing vaccine coverage levels across both diseases. Balancing the consequences of vaccination to overall health impacts, including understanding the impact of an altered mean age of infection for both chickenpox and shingles, would need to be considered prior to any vaccine introduction.
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Varicella-zoster virus (VZV) is one of the 8 herpesviruses of humans and is the cause of chickenpox (varicella) and shingles (zoster). Chickenpox, the exanthem caused by primary infection with VZV, usually occurs in children. Shingles, the clinical syndrome of segmental, unilateral, exanthem, and neuralgic pain due to reactivation of latent VZV infection, usually occurs many years after the primary infection. In the immunodeficient person, both primary and reactivated VZV infection can lead to severe generalized virus dissemination, the life-threatening form of VZV infection. The availability of antiviral agents for management of VZV infection has raised the importance of recognizing this infection in high-risk groups. Prior to the introduction of the VZV vaccine in the United States in 1995, approximately 4 million cases of chickenpox occurred each year, 83% in children younger than 9 years. There are an estimated 1 million cases of herpes zoster in the United States per year, with the annualized incidence of 1.5 to 3.0 cases per 1000 persons, and the incidence and severity of disease increases with age. A VZV vaccine was approved in 2006 for prevention of shingles in persons older than 60 years.
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Chickenpox and shingles are vaccine preventable diseases caused by varicella-zoster virus (VZV). Chickenpox is more common in children before adolescence and shingles among ≥50 years of age. With this study we aimed to determine changes in VZV epidemiology following chickenpox and shingles vaccine introduction in Queensland.This case series study used notified cases of VZV infection in Queensland from January 2010 to December 2021. In Queensland, VZV notifications are received as mostly clinically unspecified cases from pathology laboratories. Intermittent enhanced surveillance was conducted using clinician follow up to determine chickenpox and shingles clinical presentation, and we then analysed these by age-group, time period, and within vaccine eligible cohorts.Of the 87,759 VZV notifications received, 70 % (n = 61,298) were notified as unspecified, followed by 23 % shingles (n = 19,927), and 7 % chickenpox (n = 6,534). Over the study period, the percent change in total notifications adjusted by age and sex was estimated to be an increase of 5.7 % (95 % CI 4.9-6.4) each year. The chickenpox notifications fell sharply at 18 months of age (eligible for chickenpox vaccine) with the rate being 57 % and 36 % lower among those aged 18-23 months compared to <12 and 12-17 months of age, respectively. Assuming all cases aged 60 years and older were shingles, notification rates of shingles decreased by 12-22 % among 70-79 years old (eligible for shingles vaccination) over the years 2017-2021 after vaccine introduction in 2016.The VZV notification rate has increased over time in Queensland. Impact of chickenpox and shingles vaccines funded under National Immunisation Program is seen with a decline in notification rates among age-specific cohorts eligible to receive the vaccines under the program. Introduction of a second childhood dose chickenpox vaccine and more effective recombinant shingles vaccine may further improve the impact of the vaccination program.
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