BVK / SBP award for PhD thesis: "The quantitative analysis of varicella-zoster virus infection: from epidemiology to immunology".

Varicella-zoster virus (VZV) causes varicella (chickenpox) mainly in childhood and remains afterwards latent in neural ganglia. Clinical reactivation of VZV, due to reduced VZV-specific cellular immunity, causes herpes zoster (shingles). The secondary immune response following re-exposure to varicella is hypothesized to boost VZV-specific cellular immunity and thus to decrease the risk of herpes zoster in boosted individuals. Universal childhood varicella vaccination would temporary reduce the contact frequency between VZV-experienced individuals and varicella patients and thus increase the incidence of herpes zoster. As such, many countries are currently hesitant to introduce universal childhood varicella vaccination. The main goals of this PhD thesis were (1) to identify risk factors associated with VZV complications, (2) to study the dynamics of the secondary immune response following re-exposure to VZV and (3) to predict the consequences of universal childhood varicella vaccination on herpes zoster incidence by developing an individual-based population model.Using a multidisciplinary approach we were able to confirm the existence of exogenous boosting. However, both our experimental and modeling analyses presented data suggesting the individual effects of exogenous boosting to be limited to at most two years after re-exposure to varicella. Nevertheless, we predict the effects of a universal childhood varicella vaccination program on total herpes zoster incidence to be more or less the same as those by previous estimations that created hesitance amongst policy makers to implement varicella vaccination.

Keywords:VARICELLA-ZOSTER VIRUS

Disciplines:Paediatrics and neonatology, Public health care, Public health sciences, Public health services, Nursing