Integrating between-host transmission and within-host immunity to analyze the impact of varicella vaccination on zoster

Authored by Lander Willem, Philippe Beutels, Niel Hens, Benson Ogunjimi

Date Published: 2015

DOI: 10.7554/elife.07116

Sponsors: No sponsors listed

Platforms: No platforms listed

Model Documentation: Other Narrative

Model Code URLs: Model code not found

Abstract

Varicella-zoster virus (VZV) causes chickenpox and reactivation of latent VZV causes herpes zoster (HZ). VZV reactivation is subject to the opposing mechanisms of declining and boosted VZV-specific cellular mediated immunity (CMI). A reduction in exogenous re-exposure `opportunities' through universal chickenpox vaccination could therefore lead to an increase in HZ incidence. We present the first individual-based model that integrates within-host data on VZV-CMI and between-host transmission data to simulate HZ incidence. This model allows estimating currently unknown pivotal biomedical parameters, including the duration of exogenous boosting at 2 years, with a peak threefold to fourfold increase of VZV-CMI; the VZV weekly reactivation probability at 5\% and VZV subclinical reactivation having no effect on VZV-CMI. A 100\% effective chickenpox vaccine given to 1 year olds would cause a 1.75 times peak increase in HZ 31 years after implementation. This increase is predicted to occur mainly in younger age groups than is currently assumed.

Tags

HIV Infections immunization Individuals Responses Herpes-simplex-virus Subclinical reactivation Postherpetic neuralgia Chickenpox Cytomegalovirus