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We derive an exact upper bound on the epidemic overshoot for the Kermack–McKendrick SIR model. This maximal overshoot value of 0.2984 · · · occurs at$R_0^{\ast }=2.151\cdots$. In considering the utility of the notion of overshoot, a rudimentary analysis of data from the first wave of the COVID-19 pandemic in Manaus, Brazil highlights the public health hazard posed by overshoot for epidemics withR₀near 2. Using the general analysis framework presented within, we then consider more complex SIR models that incorporate vaccination.

 

Spatial systems with heterogeneities are ubiquitous in nature, from precipitation, temperature, and soil gradients controlling vegetation growth to morphogen gradients controlling gene expression in embryos. Such systems, generally described by nonlinear dynamical systems, often display complex parameter dependence and exhibit bifurcations. The dynamics of heterogeneous spatially extended systems passing through bifurcations are still relatively poorly understood, yet recent theoretical studies and experimental data highlight the resulting complex behaviors and their relevance to real-world applications. We explore the consequences of spatial heterogeneities passing through bifurcations via two examples strongly motivated by applications. These model systems illustrate that studying heterogeneity-induced behaviors in spatial systems is crucial for a better understanding of ecological transitions and functional organization in brain development. 

Infectious diseases may cause some long-term damage to their host, leading to elevated mortality even after recovery. Mortality due to complications from so-called ‘long COVID’ is a stark illustration of this potential, but the impacts of such post-infection mortality (PIM) on epidemic dynamics are not known. Using an epidemiological model that incorporates PIM, we examine the importance of this effect. We find that in contrast to mortality during infection, PIM can induce epidemic cycling. The effect is due to interference between elevated mortality and reinfection through the previously infected susceptible pool. In particular, robust immunity (via decreased susceptibility to reinfection) reduces the likelihood of cycling; on the other hand, disease-induced mortality can interact with weak PIM to generate periodicity. In the absence of PIM, we prove that the unique endemic equilibrium is stable and therefore our key result is that PIM is an overlooked phenomenon that is likely to be destabilizing. Overall, given potentially widespread effects, our findings highlight the importance of characterizing heterogeneity in susceptibility (via both PIM and robustness of host immunity) for accurate epidemiological predictions. In particular, for diseases without robust immunity, such as SARS-CoV-2, PIM may underlie complex epidemiological dynamics especially in the context of seasonal forcing.

 

Individual and societal reactions to an ongoing pandemic can lead to social dilemmas: In some cases, each individual is tempted to not follow an intervention, but for the whole society, it would be best if they did. Now that in most countries, the extent of regulations to reduce SARS-CoV-2 transmission is very small, interventions are driven by individual decision-making. Assuming that individuals act in their best own interest, we propose a framework in which this situation can be quantified, depending on the protection the intervention provides to a user and to others, the risk of getting infected, and the costs of the intervention. We discuss when a tension between individual and societal benefits arises and which parameter comparisons are important to distinguish between different regimes of intervention use.

 

Disease surveillance systems provide early warnings of disease outbreaks before they become public health emergencies. However, pandemics containment would be challenging due to the complex immunity landscape created by multiple variants. Genomic surveillance is critical for detecting novel variants with diverse characteristics and importation/emergence times. Yet, a systematic study incorporating genomic monitoring, situation assessment, and intervention strategies is lacking in the literature. We formulate an integrated computational modeling framework to study a realistic course of action based on sequencing, analysis, and response. We study the effects of the second variant’s importation time, its infectiousness advantage and, its cross-infection on the novel variant’s detection time, and the resulting intervention scenarios to contain epidemics driven by two-variants dynamics. Our results illustrate the limitation in the intervention’s effectiveness due to the variants’ competing dynamics and provide the following insights: i) There is a set of importation times that yields the worst detection time for the second variant, which depends on the first variant’s basic reproductive number; ii) When the second variant is imported relatively early with respect to the first variant, the cross-infection level does not impact the detection time of the second variant. We found that depending on the target metric, the best outcomes are attained under different interventions’ regimes. Our results emphasize the importance of sustained enforcement of Non-Pharmaceutical Interventions on preventing epidemic resurgence due to importation/emergence of novel variants. We also discuss how our methods can be used to study when a novel variant emerges within a population.

 

A key scientific challenge during the outbreak of novel infectious diseases is to predict how the course of the epidemic changes under countermeasures that limit interaction in the population. Most epidemiological models do not consider the role of mutations and heterogeneity in the type of contact events. However, pathogens have the capacity to mutate in response to changing environments, especially caused by the increase in population immunity to existing strains, and the emergence of new pathogen strains poses a continued threat to public health. Further, in the light of differing transmission risks in different congregate settings (e.g., schools and offices), different mitigation strategies may need to be adopted to control the spread of infection. We analyze a multilayer multistrain model by simultaneously accounting for i) pathways for mutations in the pathogen leading to the emergence of new pathogen strains, and ii) differing transmission risks in different settings, modeled as network layers. Assuming complete cross-immunity among strains, namely, recovery from any infection prevents infection with any other (an assumption that will need to be relaxed to deal with COVID-19 or influenza), we derive the key epidemiological parameters for the multilayer multistrain framework. We demonstrate that reductions to existing models that discount heterogeneity in either the strain or the network layers may lead to incorrect predictions. Our results highlight that the impact of imposing/lifting mitigation measures concerning different contact network layers (e.g., school closures or work-from-home policies) should be evaluated in connection with their effect on the likelihood of the emergence of new strains.

 

As the SARS-CoV-2 trajectory continues, the longer-term immuno-epidemiology of COVID-19, the dynamics of Long COVID, and the impact of escape variants are important outstanding questions. We examine these remaining uncertainties with a simple modelling framework that accounts for multiple (antigenic) exposures via infection or vaccination. If immunity (to infection or Long COVID) accumulates rapidly with the valency of exposure, we find that infection levels and the burden of Long COVID are markedly reduced in the medium term. More pessimistic assumptions on host adaptive immune responses illustrate that the longer-term burden of COVID-19 may be elevated for years to come. However, we also find that these outcomes could be mitigated by the eventual introduction of a vaccine eliciting robust (i.e. durable, transmission-blocking and/or ‘evolution-proof’) immunity. Overall, our work stresses the wide range of future scenarios that still remain, the importance of collecting real-world epidemiological data to identify likely outcomes, and the crucial need for the development of a highly effective transmission-blocking, durable and broadly protective vaccine.

 

Achieving global sustainability in the face of climate change, pandemics, and other global systemic threats will require collective intelligence and collective action beyond what we are currently experiencing. Increasing polarization within nations and populist trends that undercut international cooperation make the problem even harder. Allegiance within groups is often strengthened because of conflict among groups, leading to a form of polarization termed “affective.” Hope for addressing these global problems will require recognition of the commonality in threats facing all groups collective intelligence that integrates relevant inputs from all sources but fights misinformation and coordinated, cooperative collective action. Elinor Ostrom’s notion of polycentric governance, involving centers of decision-making from the local to the global in a complex interacting framework, may provide a possible pathway to achieve these goals.

 

A central assumption in most ecological models is that the interactions in a community operate only between pairs of species. However, two species may interactively affect the growth of a focal species. Although interactions among three or more species, called higher-order interactions, have the potential to modify our theoretical understanding of coexistence, ecologists lack clear expectations for how these interactions shape community structure. Here we analytically predict and numerically confirm how the variability and strength of higher-order interactions affect species coexistence. We found that as higher-order interaction strengths became more variable across species, fewer species could coexist, echoing the behavior of pairwise models. If interspecific higher-order interactions became too harmful relative to self-regulation, coexistence in diverse communities was destabilized, but coexistence was also lost when these interactions were too weak and mutualistic higher-order effects became prevalent. This behavior depended on the functional form of the interactions as the destabilizing effects of the mutualistic higher-order interactions were ameliorated when their strength saturated with species’ densities. Last, we showed that more species-rich communities structured by higher-order interactions lose species more readily than their species-poor counterparts, generalizing classic results for community stability. Our work provides needed theoretical expectations for how higher-order interactions impact species coexistence in diverse communities.