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Carolina J. Klett-Tammen

Publications and source records attributed to Carolina J. Klett-Tammen.

4 recordsLinked to original sources

Simulation-based inference for rapid Bayesian parameter estimation in epidemiological models: a comparison with MCMC

Mechanistic epidemiological models are widely used to support infectious disease forecasting and public-health decision making. Bayesian calibration of such models is commonly performed using Markov chain Monte Carlo (MCMC), which can become computationally expensive for high-dimensional nonlinear systems and repeated near-real-time analyses. Here, we investigate simulation-based inference (SBI) using neural posterior estimation as a scalable alternative for Bayesian calibration of a mechanistic SECIR epidemiological model using COVID-19 intensive care unit (ICU) occupancy data from Germany during 2020. We compared SBI and MCMC across multiple epidemic phases using both 31-day inference windows and a substantially more challenging 201-day reconstruction problem involving multiple transmission change points. Posterior agreement was evaluated quantitatively using Wasserstein distances and Kullback-Leibler divergences together with posterior predictive checks. Across the 31-day windows, SBI recovered posterior distributions in strong agreement with MCMC while accurately reproducing observed ICU trajectories. In the 201-day setting, SBI preserved the dominant posterior structure despite increased uncertainty. SBI, by combining CPU and GPU resources, substantially reduced computational runtime compared with MCMC, which was restricted to running on CPUs. Whereas MCMC required approximately 1000 seconds for the 31-day inference problems, SBI achieved comparable posterior and predictive performance in approximately 60-70 seconds on a single GPU. For the 201-day inference problem, SBI required an average of 157 seconds, while the MCMC runs took over 19,000 seconds. Our results demonstrate that SBI provides a rapid and computationally efficient framework for Bayesian calibration of mechanistic epidemiological models, supporting repeated near-real-time inference and rapid outbreak analysis.

cs.AI↗

Mechanics of Pandemics

COVID-19 and previous pandemics have shown how diseases can disrupt, threaten, and transform daily life. Since pathogens and societies are continuously evolving, every pandemic is different. However, certain fundamental principles of disease transmission appear to hold true across different outbreaks. These ``mechanisms'' are grounded in natural laws or the very structure of our biology and societies. This paper compiles ten fundamental mechanisms, curated by a multidisciplinary team with backgrounds spanning public health, medicine, epidemiology, political science, mathematics, physics, and psychology. These mechanisms, although perhaps underappreciated, substantially shape how pandemics unfold and are controlled. The better we succeed in understanding these mechanisms and establishing this knowledge in our societies, the better we will be able to prepare for future pandemics and respond appropriately when they occur.

q-bio.PE↗

A full software stack for epidemic disease management: Unlocking the joint potential of software technology and supercomputing

Infectious diseases remain a major threat to human societies. During the recent COVID-19 pandemic, mathematical modeling and extensive computer simulations proved highly effective in supporting public health experts and decision makers. Despite these advances, the full potential of modern modeling approaches and digital technologies has not yet been realized. Many critical tasks -- including expert consultations, model execution, scenario analyses, report preparation, and result communication -- still relied heavily on manual, human-driven processes with each manual interaction introducing avoidable delays and limiting responsiveness during rapidly evolving outbreaks. Pandemic preparedness should opt for automated workflows and seamlessly integrated software modules that can improve pandemic mitigation capabilities by substantially reducing response times. For this step, we require robust and flexible computational infrastructure capable of supporting heterogeneous hardware and continuously evolving infectious-disease models. In addition, data sources need to be dynamically integrated. Managing such demands needs infrastructure that supports automated high-performance computing (HPC) workflows. Beyond computational performance, software infrastructure must ensure secure user and data management to comply with data-protection regulations and provide clear, transparent presentation of results to both decision makers and the public. Meeting the aforementioned challenges requires tight integration of state-of-the-art scientific software with modern, scalable infrastructure that can leverage supercomputing resources when necessary. For rapid deployment in future epidemic or pandemic scenarios, adherence to the FAIR principles for research software is critical to ensure reusability and sustainability.

cs.CE↗

Testing Paradox May Explain Increased Observed Prevalence of Bacterial STIs among MSM on HIV PrEP: A Modeling Study

HIV pre-exposure Prophylaxis (PrEP) has become essential for global HIV control, but its implementation coincides with rising bacterial STI rates among men who have sex with men (MSM). While risk-compensation behavioral changes like reduced condom use are frequently reported, we examine whether intensified asymptomatic screening in PrEP programs creates surveillance artifacts that could be misinterpreted. We developed a compartmental model to represent the simultaneous spread of HIV and chlamydia (as an example of a curable STI), integrating three mechanisms: 1) risk-mediated self-protective behavior, 2) condom use reduction post-PrEP initiation, and 3) PrEP-related asymptomatic STI screening. Increasing PrEP uptake may help to reduce chlamydia prevalence, only if the PrEP-related screening is frequent enough. Otherwise, the effect of PrEP can be disadvantageous, as the drop in self-protective actions caused by larger PrEP uptake cannot be compensated for. Additionally, the change in testing behavior may lead to situations where the trend in the number of positive tests is not a reliable sign of the actual dynamics. We found a plausible mechanism to reconcile conflicting observational evidence on the effect of PrEP on STI rates, showing that simultaneous changes in testing and spreading rates may generate conflicting signals, i.e., that observed trends increase while true prevalence decreases. Asymptomatic screening, together with personalized infection treatment to minimize putative pressure to generate antibiotic resistance, is one of the key determinants of the positive side effects of PrEP in reducing STI incidence.

q-bio.PE↗