Abstract
Mass drug administration (MDA) for control of schistosomiasis is likely to affect transmission dynamics through a combination of passive vaccination and reduction of local transmission intensity. This is indicated in phenomenological models of immunity and the impact of MDA, yet immunity parameters in these models are not validated by empirical data that reflects protective immunity to reinfection. There is significant empirical evidence supporting the role of IgE in acquired protective immunity. This is proposed to be a form of delayed concomitant immunity, driven at least in part by protective IgE responses to the tegument allergen-like (TAL) family of proteins. Specific questions have arisen from modeling studies regarding the strength and duration of the protective immune response. At present, field studies have not been specifically designed to address these questions. There is therefore a need for field studies that are explicitly designed to capture epidemiological effects of acquired immunity to elucidate these immunological interactions. In doing so, it is important to address the discourse between theoretical modelers and immuno-epidemiologists and develop mechanistic models that empirically define immunity parameters. This is of increasing significance in a climate of potential changing transmission dynamics following long-term implementation of MDA.