arXiv subjects

Seba Contreras

Publications and source records attributed to Seba Contreras.

6 recordsLinked to original sources

arXiv2026

Synergistic Effects of Behavioral Feedback and Seasonality Generate Chaos in Cooperative Multi-Pathogen Systems

Infectious diseases may interact by competing for the same hosts or by facilitating subsequent infections. Understanding the dynamics of such multi-pathogen systems, particularly those subject to endemic seasonality and mitigation, is essential for designing robust public health interventions. We propose a three-stage modeling framework to disentangle the interplay between seasonality and behavioral feedback as a way of mitigation. First, we analyze a coupled susceptible-infectious-recovered-susceptible (SIRS) system without external forcing and show that the abrupt transition between the disease-free and endemic equilibria arises from a backward bifurcation-induced first-order phase transition. Second, we independently examine seasonality and behavioral feedback, characterizing where and when oscillatory behavior is induced near critical tipping points. Third, we demonstrate that their combination generates complex multi-annual wave patterns, with high-incidence cycles driven by seasonality and low-incidence intervals driven by behavioral feedback. By mapping stability as a function of seasonal forcing, mitigation strength, and cooperativity, we identify distinct period-doubling cascades with chaotic signatures arising from different mechanisms: the interplay between seasonality and behavior, and inter-pathogen cooperativity with the backward bifurcation it induces. We then analyze how these mechanisms interact across parameter ranges. Altogether, we show that cooperation fundamentally expands the spectrum of possible epidemic patterns, highlighting the importance of considering multi-pathogen interactions in epidemic modeling and control strategies.

q-bio.PE↗

arXiv2026

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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arXiv2026

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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arXiv2025

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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arXiv2025

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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arXiv2025

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 $\psi_{\rm max}$: mitigation and suppression. In the regime of (modest) mitigation, gradually increasing $\psi_{\rm max}$ 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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