Abstract
The introduction of mass vaccination against Varicella-Zoster-Virus (VZV) is being delayed in many European countries because of, among other factors, the possibility of a large increase in Herpes Zoster (HZ) incidence in the first decades after the initiation of vaccination, due to the expected decline of the boosting of Cell Mediated Immunity caused by the reduced varicella circulation. A multi-country model of VZV transmission and reactivation, is used to evaluate the possible impact of varicella vaccination on HZ epidemiology in Italy, Finland and the UK. Despite the large uncertainty surrounding HZ and vaccine-related parameters, surprisingly robust medium-term predictions are provided, indicating that an increase in HZ incidence is likely to occur in countries where the incidence rate is lower in absence of immunization, possibly due to a higher force of boosting (e.g. Finland), whereas increases in HZ incidence might be minor where the force of boosting is milder (e.g. the UK). Moreover, a convergence of HZ post vaccination incidence levels in the examined countries is predicted despite different initial degrees of success of immunization policies. Unlike previous model-based evaluations, our investigation shows that after varicella immunization an increase of HZ incidence is not a certain fact, rather depends on the presence or absence of factors promoting a strong boosting intensity and which might or not be heavily affected by changes in varicella circulation due to mass immunization. These findings might explain the opposed empirical evidences observed about the increases of HZ in sites where mass varicella vaccination is ongoing.
Highlights
Varicella, commonly referred to as chickenpox, is a highly transmissible infection caused by Varicella-Zoster-Virus (VZV), a DNA virus of the Herpes group, transmitted by direct contact with infective individuals
After recovery from varicella infection, the VZV virus remains latent in the dorsal root ganglia where it can reactivate at later ages, causing Herpes Zoster (HZ), an inflammatory skin disease, which might cause significant morbidity, including the long and painful postherpetic neuralgia [2], as well as high costs to public health payers and societies [3,4]
Still in the same paper, Hope-Simpson introduced the hypothesis of exogenous boosting, i.e. that re-exposure to VZV may be protective against HZ through boosting of Cell Mediated Immunity (CMI)
Summary
Commonly referred to as chickenpox, is a highly transmissible infection caused by Varicella-Zoster-Virus (VZV), a DNA virus of the Herpes group, transmitted by direct contact with infective individuals. The prevailing view, dating back to Hope-Simpson seminal paper, is that after temporary immunity following varicella infection, VZV reactivation may occur due to the decline of Cell Mediated Immunity (CMI) [5,6,7], e.g. as a consequence of ageing [8] or other immune-suppressing processes [9] and lead to the development of HZ. Still in the same paper, Hope-Simpson introduced the hypothesis of exogenous boosting, i.e. that re-exposure to VZV may be protective against HZ through boosting of CMI. Some controversy on this hypothesis has been raised [10], to the best of our knowledge alternative hypotheses, e.g. that boosting might follows from immunological phenomena within the individual, did not receive empirical support. Substantial evidence has accumulated in favour of ‘‘exogenous boosting hypothesis’’ from a variety of studies ranging from field studies [11], to model-based evidence [12], to Immunological and epidemiological studies [1,13]
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