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Philipp Dönges

Publications and source records attributed to Philipp Dönges.

9 recordsLinked to original sources

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.

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Household size can explain 40% of the variance in cumulative COVID-19 incidence across Europe

Household size impacts the spread of respiratory infectious diseases: Larger households tend to boost transmission by acquiring external infections more frequently and subsequently transmitting them back into the community. Furthermore, mandatory interventions primarily modulate contagion between households rather than within them. We developed an approach to quantify the role of household size in epidemics by separating within-household from out-household transmission, and found that household size explains 41% of the variability in cumulative COVID-19 incidence across 34 European countries (95% confidence interval: [15%, 46%]). The contribution of households to the overall dynamics can be quantified by a boost factor that increases with the effective household size, implying that countries with larger households require more stringent interventions to achieve the same levels of containment. This suggests that households constitute a structural (dis-)advantage that must be considered when designing and evaluating mitigation strategies.

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Stability and bifurcations of a minimal model for the effect of PrEP-related risk compensation in epidemics of sexually transmitted infections

HIV pre-exposure prophylaxis (PrEP) drastically reduces the risk of HIV infection if taken as prescribed, providing almost perfect protection even during unprotected sexual intercourse. Although this has been transformative in reducing new HIV infections among high-risk populations, it has also been linked to an increase in risk practices -- a phenomenon known as risk compensation -- thereby favoring the spread of other sexually transmitted infections (STIs) deemed less severe. In this paper, we study a minimal compartmental model describing the effect of risk awareness and risk compensation due to PrEP on the spread of other STIs among a high-infection-risk group of men who have sex with men (MSM). The model integrates three key elements of risk-mediated behavior and PrEP programs: (i) HIV risk awareness drives self-protective behaviors (such as condom use and voluntary STI screening); (ii) individuals on PrEP are subject to risk compensation, but (iii) are required to screen for asymptomatic STIs frequently. We derived the basic reproduction number of the system, $R_0$, and found a transcritical bifurcation at $R_0=1$, where the disease-free equilibrium becomes unstable and an endemic equilibrium emerges. This endemic equilibrium is asymptotically stable wherever it exists. We identified critical thresholds in behavioral and policy parameters that separate these regimes and analyzed typical values for plausible parameter choices. Beyond the specific epidemiological context, the model serves as a general framework for studying nonlinear interactions between behavioral adaptation, preventive interventions, and disease dynamics, providing insights into how feedback mechanisms can lead to non-trivial responses in epidemic systems. Finally, our model can be easily extended to study the effect of interventions and risk compensation in other STIs.

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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.

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Risk-mediated dynamic regulation of effective contacts de-synchronizes outbreaks in metapopulation epidemic models

Metapopulation epidemic models help capture the spatial dimension of infectious disease spread by dividing heterogeneous populations into separate but interconnected communities, represented by nodes in a network. In the event of an epidemic, an important research question is, to what degree spatial information (i.e., regional or national) is relevant for mitigation and (local) policymakers. This study investigates the impact of different levels of information on nationwide epidemic outcomes, modeling the reaction to the measured hazard as a feedback loop reducing contact rates in a metapopulation model based on ordinary differential equations (ODEs). Using COVID-19 and high-resolution mobility data for Germany of 2020 as a case study, we found two markedly different regimes depending on the maximum contact reduction $ψ_{\rm max}$: mitigation and suppression. In the regime of (modest) mitigation, gradually increasing $ψ_{\rm max}$ from zero to moderate levels delayed and spread out the onset of infection waves while gradually reducing the peak values. This effect was more pronounced when the contribution of regional information was low relative to national data. In the suppression regime, the feedback-induced contact reduction is strong enough to extinguish local outbreaks and decrease the mean and variance of the peak day distribution, thus regional information was more important. When suppression or elimination is impossible, ensuring local epidemics are desynchronized helps to avoid hospitalization or intensive care bottlenecks by reallocating resources from less-affected areas.

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Model-based assessment of sampling protocols for infectious disease genomic surveillance

Genomic surveillance of infectious diseases allows monitoring circulating and emerging variants and quantifying their epidemic potential. However, due to the high costs associated with genomic sequencing, only a limited number of samples can be analysed. Thus, it is critical to understand how sampling impacts the information generated. Here, we combine a compartmental model for the spread of COVID-19 (distinguishing several SARS-CoV-2 variants) with different sampling strategies to assess their impact on genomic surveillance. In particular, we compare adaptive sampling, i.e., dynamically reallocating resources between screening at points of entry and inside communities, and constant sampling, i.e., assigning fixed resources to the two locations. We show that adaptive sampling uncovers new variants up to five weeks earlier than constant sampling, significantly reducing detection delays and estimation errors. This advantage is most prominent at low sequencing rates. Although increasing the sequencing rate has a similar effect, the marginal benefits of doing so may not always justify the associated costs. Consequently, it is convenient for countries with comparatively few resources to operate at lower sequencing rates, thereby profiting the most from adaptive sampling. Finally, our methodology can be readily adapted to study undersampling in other dynamical systems.

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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.

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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.

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The winter dilemma

With winter coming in the northern hemisphere, disadvantageous seasonality of SARS-CoV-2 requires high immunity levels in the population or increasing non-pharmaceutical interventions (NPIs), compared to summer. Otherwise intensive care units (ICUs) might fill up. However, compliance with mandatory NPIs, vaccine uptake, and individual protective measures depend on individuals' opinions and behavior. Opinions, in turn, depend on information, e.g., about vaccine safety or current infection levels. Therefore, understanding how information about the pandemic affects its spread through the modulation of voluntary protection-seeking behaviors is crucial for better preparedness this winter and for future crises.

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