arXiv subjects

Jonas Dehning

Publications and source records attributed to Jonas Dehning.

14 recordsLinked to original sources

arXiv2025

Optimizing infectious disease mitigation under dynamic conditions

Mitigation measures are essential for controlling the spread of infectious diseases during pandemics and epidemics, but they impose considerable societal, individual, and economic costs. We developed a general optimization framework to balance costs related to infection and to mitigation. Optimizing the trade-off between mitigation and infection cost, we identified three novel, surprising effects: First, assuming a constant reproduction number $R_0$, the optimal response to an infectious disease requires either strict mitigation or none at all, depending on disease severity, but never does one find an intermediate mitigation level to be optimal. Second, under seasonal variations, optimal mitigation is stricter during winter. Interestingly, a single wave of infections still arises in spring with 3 months delay to the seasonal peak of infectivity, replacing the autumn/winter waves known for classical influenza. Third, during steady vaccination campaigns, even optimal mitigation can result in transient infection waves. Finally, we quantify the cost of delayed mitigation onset and show that even short delays can substantially increase total costs -- if the disease is severe. Overall, our framework is easily applicable to general and complex settings and thereby presents a versatile tool to explore optimal mitigation strategies for endemic and pandemic infectious disease.

q-bio.PE↗

arXiv2025

Inferring Mobility Reductions from COVID-19 Disease Spread along the Urban-Rural Gradient

The COVID-19 pandemic reshaped human mobility through policy interventions and voluntary behavioral changes. Mobility adaptions helped mitigate pandemic spread, however our knowledge which environmental, social, and demographic factors helped mobility reduction and pandemic mitigation is patchy. We introduce a Bayesian hierarchical model to quantify heterogeneity in mobility responses across time and space in Germany's 400 districts using anonymized mobile phone data. Decomposing mobility into a disease-responsive component and disease-independent factors (temperature, school vacations, public holidays) allows us to quantify the impact of each factor. We find significant differences in reaction to disease spread along the urban-rural gradient, with large cities reducing mobility most strongly. Employment sectors further help explain variance in reaction strength during the first wave, while political variables gain significance during the second wave. However, reduced mobility only partially translates to lower peak incidence, indicating the influence of other hidden factors. Our results identify key drivers of mobility reductions and demonstrate that mobility behavior can serve as an operational proxy for population response.

stat.AP↗

arXiv2023

How contact patterns destabilize and modulate epidemic outbreaks

The spread of a contagious disease clearly depends on when infected individuals come into contact with susceptible ones. Such effects, however, have remained largely unexplored in the study of epidemic outbreaks. In particular, it remains unclear how the timing of contacts interacts with the latent and infectious stages of the disease. Here, we use real-world physical proximity data to study this interaction and find that the temporal statistics of actual human contact patterns i) destabilize epidemic outbreaks and ii) modulate the basic reproduction number. We explain both observations by distinct aspects of the observed contact patterns. On the one hand, we find the destabilization of outbreaks to be caused by temporal clustering of contacts leading to over-dispersed offspring distributions and increased probabilities of otherwise rare events (zero- and super-spreading). Notably, our analysis enables us to disentangle previously elusive sources of over-dispersion in empirical offspring distributions. On the other hand, we find the modulation of R0 to be caused by a periodically varying contact rate. Both mechanisms are a direct consequence of the memory in contact behavior, and we showcase a generative process that reproduces these non-Markovian statistics. Our results point to the importance of including non-Markovian contact timings into studies of epidemic outbreaks.

physics.soc-ph↗

arXiv2023

Impact of the Euro 2020 championship on the spread of COVID-19

Large-scale events like the UEFA Euro~2020 football (soccer) championship offer a unique opportunity to quantify the impact of gatherings on the spread of COVID-19, as the number and dates of matches played by participating countries resembles a randomized study. Using Bayesian modeling and the gender imbalance in COVID-19 data, we attribute 840,000 (95% CI: [0.39M, 1.26M]) COVID-19 cases across 12 countries to the championship. The impact depends non-linearly on the initial incidence, the reproduction number $R$, and the number of matches played. The strongest effects are seen in Scotland and England, where as much as 10,000 primary cases per million inhabitants occur from championship-related gatherings. The average match-induced increase in $R$ was 0.46 [0.18, 0.75] on match days, but important matches caused an increase as large as +3. Altogether, our results provide quantitative insights that help judge and mitigate the impact of large-scale events on pandemic spread.

q-bio.PE↗

arXiv2022

Evaluating vaccine allocation strategies using simulation-assisted causal modelling

Early on during a pandemic, vaccine availability is limited, requiring prioritisation of different population groups. Evaluating vaccine allocation is therefore a crucial element of pandemics response. In the present work, we develop a model to retrospectively evaluate age-dependent counterfactual vaccine allocation strategies against the COVID-19 pandemic. To estimate the effect of allocation on the expected severe-case incidence, we employ a simulation-assisted causal modelling approach which combines a compartmental infection-dynamics simulation, a coarse-grained, data-driven causal model and literature estimates for immunity waning. We compare Israel's implemented vaccine allocation strategy in 2021 to counterfactual strategies such as no prioritisation, prioritisation of younger age groups or a strict risk-ranked approach; we find that Israel's implemented strategy was indeed highly effective. We also study the marginal impact of increasing vaccine uptake for a given age group and find that increasing vaccinations in the elderly is most effective at preventing severe cases, whereas additional vaccinations for middle-aged groups reduce infections most effectively. Due to its modular structure, our model can easily be adapted to study future pandemics. We demonstrate this flexibility by investigating vaccine allocation strategies for a pandemic with characteristics of the Spanish Flu. Our approach thus helps evaluate vaccination strategies under the complex interplay of core epidemic factors, including age-dependent risk profiles, immunity waning, vaccine availability and spreading rates.

stat.AP↗

arXiv2022

Intrinsic timescales of spiking activity in humans during wakefulness and sleep

Information processing in the brain requires integration of information over time. Such an integration can be achieved if signals are maintained in the network activity for the required period, as quantified by the intrinsic timescale. While short timescales are considered beneficial for fast responses to stimuli, long timescales facilitate information storage and integration. We quantified intrinsic timescales from spiking activity in the medial temporal lobe of humans. We found extended and highly diverse timescales ranging from tens to hundreds of milliseconds, though with no evidence for differences between subareas. Notably, however, timescales differed between sleep stages and were longest during slow wave sleep. This supports the hypothesis that intrinsic timescales are a central mechanism to tune networks to the requirements of different tasks and cognitive states.

q-bio.NC↗

arXiv2022

Interplay between risk perception, behaviour, and COVID-19 spread

Pharmaceutical and non-pharmaceutical interventions (NPIs) have been crucial for controlling COVID-19. They are complemented by voluntary health-protective behaviour, building a complex interplay between risk perception, behaviour, and disease spread. We studied how voluntary health-protective behaviour and vaccination willingness impact the long-term dynamics. We analysed how different levels of mandatory NPIs determine how individuals use their leeway for voluntary actions. If mandatory NPIs are too weak, COVID-19 incidence will surge, implying high morbidity and mortality before individuals react; if they are too strong, one expects a rebound wave once restrictions are lifted, challenging the transition to endemicity. Conversely, moderate mandatory NPIs give individuals time and room to adapt their level of caution, mitigating disease spread effectively. When complemented with high vaccination rates, this also offers a robust way to limit the impacts of the Omicron variant of concern. Altogether, our work highlights the importance of appropriate mandatory NPIs to maximise the impact of individual voluntary actions in pandemic control.

q-bio.PE↗

arXiv2021

Low case numbers enable long-term stable pandemic control without lockdowns

The traditional long-term solutions for epidemic control involve eradication or population immunity. Here, we analytically derive the existence of a third viable solution: a stable equilibrium at low case numbers, where test-trace-and-isolate policies partially compensate for local spreading events, and only moderate restrictions remain necessary. In this equilibrium, daily cases stabilize around ten new infections per million people or less. However, stability is endangered if restrictions are relaxed or case numbers grow too high. The latter destabilization marks a tipping point beyond which the spread self-accelerates. We show that a lockdown can reestablish control and that recurring lockdowns are not necessary given sustained, moderate contact reduction. We illustrate how this strategy profits from vaccination and helps mitigate variants of concern. This strategy reduces cumulative cases (and fatalities) 4x more than strategies that only avoid hospital collapse. In the long term, immunization, large-scale testing, and international coordination will further facilitate control.

q-bio.PE↗

arXiv2021

Mutational signatures and transmissibility of SARS-CoV-2 Gamma and Lambda variants

The emergence of SARS-CoV-2 variants of concern endangers the long-term control of COVID-19, especially in countries with limited genomic surveillance. In this work, we explored genomic drivers of contagion in Chile. We sequenced 3443 SARS-CoV-2 genomes collected between January and July 2021, where the Gamma (P.1), Lambda (C.37), Alpha (B.1.1.7), B.1.1.348, and B.1.1 lineages were predominant. Using a Bayesian model tailored for limited genomic surveillance, we found that Lambda and Gamma variants' reproduction numbers were about 5% and 16% larger than Alpha's, respectively. We observed an overabundance of mutations in the Spike gene, strongly correlated with the variant's transmissibility. Furthermore, the variants' mutational signatures featured a breakpoint concurrent with the beginning of vaccination (mostly CoronaVac, an inactivated virus vaccine), indicating an additional putative selective pressure. Thus, our work provides a reliable method for quantifying novel variants' transmissibility under subsampling (as newly-reported Delta, B.1.617.2) and highlights the importance of continuous genomic surveillance.

q-bio.PE↗

arXiv2021

Relaxing restrictions at the pace of vaccination increases freedom and guards against further COVID-19 waves

Mass vaccination offers a promising exit strategy for the COVID-19 pandemic. However, as vaccination progresses, demands to lift restrictions increase, despite most of the population remaining susceptible. Using our age-stratified SEIRD-ICU compartmental model and curated epidemiological and vaccination data, we quantified the rate (relative to vaccination progress) at which countries can lift non-pharmaceutical interventions without overwhelming their healthcare systems. We analyzed scenarios ranging from immediately lifting restrictions (accepting high mortality and morbidity) to reducing case numbers to a level where test-trace-and-isolate (TTI) programs efficiently compensate for local spreading events. In general, the age-dependent vaccination roll-out implies a transient decrease of more than ten years in the average age of ICU patients and deceased. The pace of vaccination determines the speed of lifting restrictions; Taking the European Union (EU) as an example case, all considered scenarios allow for steadily increasing contacts starting in May 2021 and relaxing most restrictions by autumn 2021. Throughout summer 2021, only mild contact restrictions will remain necessary. However, only high vaccine uptake can prevent further severe waves. Across EU countries, seroprevalence impacts the long-term success of vaccination campaigns more strongly than age demographics. In addition, we highlight the need for preventive measures to reduce contagion in school settings throughout the year 2021, where children might be drivers of contagion because of them remaining susceptible...

q-bio.PE↗

arXiv2020

The challenges of containing SARS-CoV-2 via test-trace-and-isolate

Without a cure, vaccine, or proven long-term immunity against SARS-CoV-2, test-trace-and-isolate (TTI) strategies present a promising tool to contain its spread. For any TTI strategy, however, mitigation is challenged by pre- and asymptomatic transmission, TTI-avoiders, and undetected spreaders, who strongly contribute to hidden infection chains. Here, we studied a semi-analytical model and identified two tipping points between controlled and uncontrolled spread: (1) the behavior-driven reproduction number of the hidden chains becomes too large to be compensated by the TTI capabilities, and (2) the number of new infections exceeds the tracing capacity. Both trigger a self-accelerating spread. We investigated how these tipping points depend on challenges like limited cooperation, missing contacts, and imperfect isolation. Our model results suggest that TTI alone is insufficient to contain an otherwise unhindered spread of SARS-CoV-2, implying that complementary measures like social distancing and improved hygiene remain necessary.

q-bio.PE↗

arXiv2020

The foreshadow of a second wave: An analysis of current COVID-19 fatalities in Germany

A second wave of SARS-CoV-2 is unfolding in dozens of countries. However, this second wave manifests itself strongly in new reported cases, but less in death counts compared to the first wave. Over the past three months in Germany, the reported cases increased by a factor five or more, whereas the death counts hardly grew. This discrepancy fueled speculations that the rise of reported cases would not reflect a second wave but only wider testing. We find that this apparent discrepancy can be explained to a large extent by the age structure of the infected, and predict a pronounced increase of death counts in the near future, as the spread once again expands into older age groups. To re-establish control, and to avoid the tipping point when TTI capacity is exceeded, case numbers have to be lowered. Otherwise the control of the spread and the protection of vulnerable people will require more restrictive measures latest when the hospital capacity is reached.

q-bio.PE↗

arXiv2020

Inferring change points in the COVID-19 spreading reveals the effectiveness of interventions

As COVID-19 is rapidly spreading across the globe, short-term modeling forecasts provide time-critical information for decisions on containment and mitigation strategies. A main challenge for short-term forecasts is the assessment of key epidemiological parameters and how they change when first interventions show an effect. By combining an established epidemiological model with Bayesian inference, we analyze the time dependence of the effective growth rate of new infections. Focusing on the COVID-19 spread in Germany, we detect change points in the effective growth rate that correlate well with the times of publicly announced interventions. Thereby, we can quantify the effect of interventions, and we can incorporate the corresponding change points into forecasts of future scenarios and case numbers. Our code is freely available and can be readily adapted to any country or region.

q-bio.PE↗

arXiv2018

Dynamic Adaptive Computation: Tuning network states to task requirements

Neural circuits are able to perform computations under very diverse conditions and requirements. The required computations impose clear constraints on their fine-tuning: a rapid and maximally informative response to stimuli in general requires decorrelated baseline neural activity. Such network dynamics is known as asynchronous-irregular. In contrast, spatio-temporal integration of information requires maintenance and transfer of stimulus information over extended time periods. This can be realized at criticality, a phase transition where correlations, sensitivity and integration time diverge. Being able to flexibly switch, or even combine the above properties in a task-dependent manner would present a clear functional advantage. We propose that cortex operates in a "reverberating regime" because it is particularly favorable for ready adaptation of computational properties to context and task. This reverberating regime enables cortical networks to interpolate between the asynchronous-irregular and the critical state by small changes in effective synaptic strength or excitation-inhibition ratio. These changes directly adapt computational properties, including sensitivity, amplification, integration time and correlation length within the local network. We review recent converging evidence that cortex in vivo operates in the reverberating regime, and that various cortical areas have adapted their integration times to processing requirements. In addition, we propose that neuromodulation enables a fine-tuning of the network, so that local circuits can either decorrelate or integrate, and quench or maintain their input depending on task. We argue that this task-dependent tuning, which we call "dynamic adaptive computation", presents a central organization principle of cortical networks and discuss first experimental evidence.

q-bio.NC↗