RTI uses cookies to offer you the best experience online. By clicking “accept” on this website, you opt in and you agree to the use of cookies. If you would like to know more about how RTI uses cookies and how to manage them please view our Privacy Policy here. You can “opt out” or change your mind by visiting: http://optout.aboutads.info/. Click “accept” to agree.
Modeling the impact of exogenous boosting on herpes zoster
an updated methodological review of the varicella zoster virus literature
Talbird, S., La, E., Mauskopf, J., Krueger, W., Altland, A., & Daniels, VJ. (2017). Modeling the impact of exogenous boosting on herpes zoster: an updated methodological review of the varicella zoster virus literature. Value in Health, 20(5), A325. https://doi.org/10.1016/j.jval.2017.05.005
OBJECTIVES: Historically, mathematical models of the impact of universal childhood varicella vaccination (UVV) have used limited data to capture effects of exogenous boosting (EB). EB posits that cell-mediated immunity (CMI) is boosted for individuals re-exposed to varicella zoster virus (VZV), leading models to often conclude that UVV will cause a temporary herpes zoster (HZ) increase. Our objective was to update a previous literature review (Ogunjimi et al., 2013) to summarize any new evidence from observational or modeling studies related to EB and its parameterization.
METHODS: Electronic searches of two databases and seven congresses were performed using the previous review’s published search strategies. Identified studies were screened to determine inclusion eligibility and to identify additional sources. Data on observational study designs and mathematical model structures, EB frameworks, and HZ-related parameter values were abstracted, with results synthesized.
RESULTS: The updated review identified 29 additional studies. Among 17 observational studies, 8 analyses included both pre- and post-UVV data in 4 countries. Most analyses (n¼6) reported pre-UVV increases in HZ incidence, making it difficult to attribute post-UVV increases to UVV versus other causes. Among 12 modeling studies, various EB frameworks were considered, ranging from no EB to full permanent immunity; the progressive immunity framework (i.e., CMI increases for a proportion of VZV exposures and accumulates after each exposure) best captured EB based on statistical fit to realworld pre-UVV data. HZ-related parameter values varied widely by study/country, even for biologically-based parameters (e.g., CMI duration); assumed HZ-related parameter values for vaccinated individuals were similar. Other key factors affecting post-UVV HZ incidence included population contact patterns, demographic changes over time, and pre-UVV HZ incidence. CONCLUSIONS: New methods for incorporating EB into mathematical models may better capture EB than previous approaches, although further research on the biological processes and resulting effects of EB on HZ incidence is needed.
