Supplementary Materials Supporting Information supp_108_17_7259__index. age-organized model that encapsulates this hypothesis. We discover that immune improving must be more easily triggered than main infection to account for age-incidence data. We make age-specific and dynamical predictions through bifurcation analysis and simulation. The boosting model proposed here parsimoniously captures four important features of pertussis data from highly vaccinated countries: (Instances identified between 1918 and 1921, with instances aggregated into twelve age groups KRN 633 ic50 (year very long from 0 to 10?years of age, then 10C15, and ?15). (in adults have led to a rise in diagnoses but not true disease incidence. However, the frequent, pronounced, and highly symptomatic outbreaks within high universities over the past two decades have established this phenomenon as a switch in illness patterns, not merely diagnostics (5). (away KRN 633 ic50 from the original vaccine-targeted strain (18, 19). The evidence for this is definitely inconclusive, with one study finding that has not exhibited accelerated evolutionary rates that would be indicative of positive selection (20) and others finding that there is definitely evidence of high levels of polymorphism in antigenic sites, suggestive of positive selection driven by interactions with sponsor immunity (18). Whereas vaccine-driven evolution may help to explain the increase in total incidence, it can not explain the shift in age-specific incidence (Fig.?1can exhibit boosting of antibody titers, without developing medical symptoms merlin (9, 25C27). In addition, studies on vaccine efficacy have shown that the pertussis booster vaccine (Adacel) elicits a significantly stronger immune response than the main vaccine (Daptacel) despite containing five instances less pertussis toxin (28). This is to be expected because immune memory space cells respond more quickly and to lower doses of antigen when primed than when naive (29, 30). Recent improvements in imaging systems have made it possible to observe the kinetics of primed, tolerized and naive T cells in response to antigenic stimulation in vivo and demonstrated that primed T cells are more efficient at identifying and responding to antigen presenting cells than naive ones (31, 32). This suggests that a brief exposure to a small amount of antigen can restimulate immunity, extending its efficacy without causing symptomatic or transmissible infection. We herein refer to this phenomenon as immune boosting. Previous work has explored the effects of immune boosting on disease dynamics in general, and pertussis in particular (33, 34). However, in previous models of disease transmission, this phenomenon has generally been presumed to be no more likely than primary infection (21, 35C37). The model analyzed here incorporates immunological evidence on the sensitivity and speed of primed B and T cells by allowing individuals who are reexposed to antigens to generate an immune response to a more casual contact than would be necessary to cause a primary infection. This allows our model to capture the age-specific incidence in both the pre- and postvaccine eras using estimates of the immune duration that are in KRN 633 ic50 accord with clinical evidence. There have been many models that incorporate loss of immunity and reexposure in an attempt to understand the pre- or postvaccine era data. One model has predicted the recent rise in cases as a consequence of a contrast between permanent infection-induced immunity and shorter-lived vaccine-induced immunity (4). However, it is becoming increasingly clear that immunity to both natural infection and vaccination wanes with.