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Purpose of Review: Type 1 diabetes impacts 1.3 million people in the USA with a total direct lifetime medical cost of $133.7 billion. Management requires a mix of daily exogenous insulin administration and frequent glucose monitoring. Decision-making by the individual can be burdensome. Recent Findings: Beta-cell replacement, which involves devices protecting cells from autoimmunity and allo-rejection, aims at restoring physiological glucose regulation and improving clinical outcomes in patients. Given the significant burden of T1D in the healthcare systems, cost-effectiveness analyses can drive innovation and policymaking in the area. Summary: This review presents the health economics analyses performed for donor-derived islet transplantation and the possible outcomes of stem cell-derived beta cells. Long-term cost-effectiveness of islet transplantation depends on the engraftment of these transplants, and the expenses and thresholds assumed by healthcare systems in different countries. Early health technology assessment analyses for stem cell-derived beta-cell replacement suggest manufacturing optimization is necessary to reduce upfront costs.

After remarkable success of vector control campaigns worldwide, concerns about loss of immunity against Plasmodium falciparum due to lack of exposure to the parasite are relevant since an increase of severe cases in less immune individuals is expected. We present a mathematical model to investigate the impact of reducing exposure to the parasite on the immune repertoire against P. falciparum erythrocyte membrane protein 1 (PfEMP1) variants. The model was parameterized with data from Príncipe Island, West Africa, and applied to simulate two alternative transmission scenarios: one where control measures are continued to eventually drive the system to elimination; and another where the effort is interrupted after 6 years of its initiation and the system returns to the initial transmission potential. Population dynamics of parasite prevalence predict that in a few years infection levels return to the pre-control values, while the re-acquisition of the immune repertoire against PfEMP1 is slower, creating a window for increased severity. The model illustrates the consequences of loss of immune repertoire against PfEMP1 in a given setting and can be applied to other regions where similar data may be available.