Spatiotemporal dynamics in a fractional diffusive SIS epidemic model with mass action infection mechanism.

This paper is concerned with spatiotemporal dynamics of a fractional diffusive susceptible-infected-susceptible (SIS) epidemic model with mass action infection mechanism. Concretely, we first focus on the existence and stability of the disease-free and endemic equilibria. Then, we give the asymptotic profiles of the endemic equilibrium on small and large diffusion rates, which can reveal the impact of dispersal rates and fractional powers simultaneously. It is worth noting that we have some counter-intuitive findings: controlling the flow of infected individuals will not eradicate the disease, but restricting the movement of susceptible individuals will make the disease disappear.

Managing spatio-temporal heterogeneity of susceptibles by embedding it into an homogeneous model: A mechanistic and deep learning study.

Accurate prediction of epidemics is pivotal for making well-informed decisions for the control of infectious diseases, but addressing heterogeneity in the system poses a challenge. In this study, we propose a novel modelling framework integrating the spatio-temporal heterogeneity of susceptible individuals into homogeneous models, by introducing a continuous recruitment process for the susceptibles. A neural network approximates the recruitment rate to develop a Universal Differential Equations (UDE) model. Simultaneously, we pre-set a specific form for the recruitment rate and develop a mechanistic model. Data from a COVID Omicron variant outbreak in Shanghai are used to train the UDE model using deep learning methods and to calibrate the mechanistic model using MCMC methods. Subsequently, we project the attack rate and peak of new infections for the first Omicron wave in China after the adjustment of the dynamic zero-COVID policy. Our projections indicate an attack rate and a peak of new infections of 80.06% and 3.17% of the population, respectively, compared with the homogeneous model's projections of 99.97% and 32.78%, thus providing an 18.6% improvement in the prediction accuracy based on the actual data. Our simulations demonstrate that heterogeneity in the susceptibles decreases herd immunity for ~37.36% of the population and prolongs the outbreak period from ~30 days to ~70 days, also aligning with the real case. We consider that this study lays the groundwork for the development of a new class of models and new insights for modelling heterogeneity.

An SIS epidemic model with individual variation.

We study an extension of the stochastic SIS (Susceptible-Infectious-Susceptible) model in continuous time that accounts for variation amongst individuals. By examining its limiting behaviour as the population size grows we are able to exhibit conditions for the infection to become endemic.

Modelling the impact of precaution on disease dynamics and its evolution.

In this paper, we introduce the notion of practically susceptible population, which is a fraction of the biologically susceptible population. Assuming that the fraction depends on the severity of the epidemic and the public's level of precaution (as a response of the public to the epidemic), we propose a general framework model with the response level evolving with the epidemic. We firstly verify the well-posedness and confirm the disease's eventual vanishing for the framework model under the assumption that the basic reproduction number R 0 < 1 . For R 0 > 1 , we study how the behavioural response evolves with epidemics and how such an evolution impacts the disease dynamics. More specifically, when the precaution level is taken to be the instantaneous best response function in literature, we show that the endemic dynamic is convergence to the endemic equilibrium; while when the precaution level is the delayed best response, the endemic dynamic can be either convergence to the endemic equilibrium, or convergence to a positive periodic solution. Our derivation offers a justification/explanation for the best response used in some literature. By replacing "adopting the best response" with "adapting toward the best response", we also explore the adaptive long-term dynamics.

A risk-induced dispersal strategy of the infected population for a disease-free state in the SIS epidemic model.

This article proposes a dispersal strategy for infected individuals in a spatial susceptible-infected-susceptible (SIS) epidemic model. The presence of spatial heterogeneity and the movement of individuals play crucial roles in determining the persistence and eradication of infectious diseases. To capture these dynamics, we introduce a moving strategy called risk-induced dispersal (RID) for infected individuals in a continuous-time patch model of the SIS epidemic. First, we establish a continuous-time n-patch model and verify that the RID strategy is an effective approach for attaining a disease-free state. This is substantiated through simulations conducted on 7-patch models and analytical results derived from 2-patch models. Second, we extend our analysis by adapting the patch model into a diffusive epidemic model. This extension allows us to explore further the impact of the RID movement strategy on disease transmission and control. We validate our results through simulations, which provide the effects of the RID dispersal strategy.

Heterogeneous risk attitudes and waves of infection.

Many countries have experienced multiple waves of infection during the COVID-19 pandemic. We propose a novel but parsimonious extension of the SIR model, a CSIR model, that can endogenously generate waves. In the model, cautious individuals take appropriate prevention measures against the virus and are not exposed to infection risk. Incautious individuals do not take any measures and are susceptible to the risk of infection. Depending on the size of incautious and susceptible population, some cautious people lower their guard and become incautious-thus susceptible to the virus. When the virus spreads sufficiently, the population reaches "temporary" herd immunity and infection subsides thereafter. Yet, the inflow from the cautious to the susceptible eventually expands the susceptible population and leads to the next wave. We also show that the CSIR model is isomorphic to the SIR model with time-varying parameters.

Final epidemic size of a two-community SIR model with asymmetric coupling.

Communities are commonly not isolated but interact asymmetrically with each other, allowing the propagation of infectious diseases within the same community and between different communities. To reveal the impact of asymmetrical interactions and contact heterogeneity on disease transmission, we formulate a two-community SIR epidemic model, in which each community has its contact structure while communication between communities occurs through temporary commuters. We derive an explicit formula for the basic reproduction number R 0 , give an implicit equation for the final epidemic size z, and analyze the relationship between them. Unlike the typical positive correlation between R 0 and z in the classic SIR model, we find a negatively correlated relationship between counterparts of our model deviating from homogeneous populations. Moreover, we investigate the impact of asymmetric coupling mechanisms on R 0 . The results suggest that, in scenarios with restricted movement of susceptible individuals within a community, R 0 does not follow a simple monotonous relationship, indicating that an unbending decrease in the movement of susceptible individuals may increase R 0 . We further demonstrate that network contacts within communities have a greater effect on R 0 than casual contacts between communities. Finally, we develop an epidemic model without restriction on the movement of susceptible individuals, and the numerical simulations suggest that the increase in human flow between communities leads to a larger R 0 .

General protocol for predicting outbreaks of infectious diseases in social networks.

Epidemic spreading on social networks with quenched connections is strongly influenced by dynamic correlations between connected nodes, posing theoretical challenges in predicting outbreaks of infectious diseases. The quenched connections introduce dynamic correlations, indicating that the infection of one node increases the likelihood of infection among its neighboring nodes. These dynamic correlations pose significant difficulties in developing comprehensive theories for threshold determination. Determining the precise epidemic threshold is pivotal for diseases control. In this study, we propose a general protocol for accurately determining epidemic thresholds by introducing a new set of fundamental conditions, where the number of connections between individuals of each type remains constant in the stationary state, and by devising a rescaling method for infection rates. Our general protocol is applicable to diverse epidemic models, regardless of the number of stages and transmission modes. To validate our protocol's effectiveness, we apply it to two widely recognized standard models, the susceptible-infected-recovered-susceptible model and the contact process model, both of which have eluded precise threshold determination using existing sophisticated theories. Our results offer essential tools to enhance disease control strategies and preparedness in an ever-evolving landscape of infectious diseases.

Final epidemic size and critical times for susceptible-infectious-recovered models with a generalized contact rate.

During the spread of an infectious disease, the contact rate or the incidence rate may affect disease characteristics. For simplicity, most disease models assume standard incidence or mass action rates to calculate the basic reproduction number, final epidemic size, and peak time of an epidemic. For standard incidence, the contact rate remains constant resulting in the incidence rate is inversely proportional to the population size, while for the mass action rate, this contact rate is proportional to the total population size resulting in the incidence rate is independent of the population size. In this paper, we consider susceptible-infectious-recovered epidemic models with a generalized contact rate C(N) and a nonlinear incidence rate in view of the behavioral change from susceptible or infectious individuals when an infectious disease appears. The basic reproduction number and the final size equation are derived. The impact of different types of contact rates on them is studied. Moreover, two critical times (peak time and epidemic duration) of an epidemic are considered. Explicit formulas for the peak time and epidemic duration are obtained. These formulas are helpful not only for taking early effective epidemic precautions but also for understanding how the epidemic duration can be changed by acting on the model parameters, especially when the epidemic model is used to make public health policy.

Susceptible-Infected-Susceptible type COVID-19 spread with collective effects.

Many models developed to forecast and attempt to understand the COVID-19 pandemic are highly complex, and few take collective behavior into account. As the pandemic progressed individual recurrent infection was observed and simpler susceptible-infected type models were introduced. However, these do not include mechanisms to model collective behavior. Here, we introduce an extension of the SIS model that accounts for collective behavior and show that it has four equilibria. Two of the equilibria are the standard SIS model equilibria, a third is always unstable, and a fourth where collective behavior and infection prevalence interact to produce either node-like or oscillatory dynamics. We then parameterized the model using estimates of the transmission and recovery rates for COVID-19 and present phase diagrams for fixed recovery rate and free transmission rate, and both rates fixed. We observe that regions of oscillatory dynamics exist in both cases and that the collective behavior parameter regulates their extent. Finally, we show that the system exhibits hysteresis when the collective behavior parameter varies over time. This model provides a minimal framework for explaining oscillatory phenomena such as recurring waves of infection and hysteresis effects observed in COVID-19, and other SIS-type epidemics, in terms of collective behavior.

Monitoring COVID-19 pandemic in Saudi Arabia using SEIRD model parameters with MEWMA.

BACKGROUND: When the COVID-19 pandemic hit Saudi Arabia, decision-makers were confronted with the difficult task of implementing treatment and disease prevention measures. To make effective decisions, officials must monitor several pandemic attributes simultaneously. Such as spreading rate, which is the number of new cases of a disease compared to existing cases; infection rate refers to how many cases have been reported in the entire population, and the recovery rate, which is how effective treatment is and indicates how many people recover from an illness and the mortality rate is how many deaths there are for every 10,000 people. METHODS: Based on a Susceptible, Exposed, Infected, Recovered Death (SEIRD) model, this study presents a method for monitoring changes in the dynamics of a pandemic. This approach uses a Bayesian paradigm for estimating the parameters at each time using a particle Markov chain Monte Carlo (MCMC) method. The MCMC samples are then analyzed using Multivariate Exponentially Weighted Average (MEWMA) profile monitoring technique, which will "signal" if a change in the SEIRD model parameters change. RESULTS: The method is applied to the pre-vaccine COVID-19 data for Saudi Arabia and the MEWMA process shows changes in parameter profiles which correspond to real world events such as government interventions or changes in behaviour. CONCLUSIONS: The method presented here is a tool that researchers and policy makers can use to monitor pandemics in a real time manner.

Characterization of differential susceptibility and differential infectivity epidemic models.

Heterogeneity in susceptibility and infectivity is a central issue in epidemiology. Although the latter has received some attention recently, the former is often neglected in modeling of epidemic systems. Moreover, very few studies consider both of these heterogeneities. This paper is concerned with the characterization of epidemic models with differential susceptibility and differential infectivity under a general setup. Specifically, we investigate the global asymptotic behavior of equilibria of these systems when the network configuration of the Susceptible-Infectious interactions is strongly connected. These results prove two conjectures by Bonzi et al. (J Math Biol 62:39-64, 2011) and Hyman and Li (Math Biosci Eng 3:89-100, 2006). Moreover, we consider the scenario in which the strong connectivity hypothesis is dropped. In this case, the model exhibits a wider range of dynamical behavior, including the rise of boundary and interior equilibria, all based on the topology of network connectivity. Finally, a model with multidirectional transitions between infectious classes is presented and completely analyzed.

Consumers Can Now Buy a Blood Test to Evaluate Their Alzheimer Disease Risk, but Should They?

This Medical News feature discusses a Quest Diagnostics blood biomarkers test that is supposed to help consumers assess their Alzheimer disease risk.

Necessary and sufficient conditions for exact closures of epidemic equations on configuration model networks.

We prove that it is possible to obtain the exact closure of SIR pairwise epidemic equations on a configuration model network if and only if the degree distribution follows a Poisson, binomial, or negative binomial distribution. The proof relies on establishing the equivalence, for these specific degree distributions, between the closed pairwise model and a dynamical survival analysis (DSA) model that was previously shown to be exact. Specifically, we demonstrate that the DSA model is equivalent to the well-known edge-based Volz model. Using this result, we also provide reductions of the closed pairwise and Volz models to a single equation that involves only susceptibles. This equation has a useful statistical interpretation in terms of times to infection. We provide some numerical examples to illustrate our results.

Large-deviations of disease spreading dynamics with vaccination.

We numerically simulated the spread of disease for a Susceptible-Infected-Recovered (SIR) model on contact networks drawn from a small-world ensemble. We investigated the impact of two types of vaccination strategies, namely random vaccination and high-degree heuristics, on the probability density function (pdf) of the cumulative number C of infected people over a large range of its support. To obtain the pdf even in the range of probabilities as small as 10-80, we applied a large-deviation approach, in particular the 1/t Wang-Landau algorithm. To study the size-dependence of the pdfs within the framework of large-deviation theory, we analyzed the empirical rate function. To find out how typical as well as extreme mild or extreme severe infection courses arise, we investigated the structures of the time series conditioned to the observed values of C.

Modeling the effects of Prophylactic behaviors on the spread of SARS-CoV-2 in West Africa.

Various general and individual measures have been implemented to limit the spread of SARS-CoV-2 since its emergence in China. Several phenomenological and mechanistic models have been developed to inform and guide health policy. Many of these models ignore opinions about certain control measures, although various opinions and attitudes can influence individual actions. To account for the effects of prophylactic opinions on disease dynamics and to avoid identifiability problems, we expand the SIR-Opinion model of Tyson et al. (2020) to take into account the partial detection of infected individuals in order to provide robust modeling of COVID-19 as well as degrees of adherence to prophylactic treatments, taking into account a hybrid modeling technique using Richard's model and the logistic model. Applying the approach to COVID-19 data from West Africa demonstrates that the more people with a strong prophylactic opinion, the smaller the final COVID-19 pandemic size. The influence of individuals on each other and from the media significantly influences the susceptible population and, thus, the dynamics of the disease. Thus, when considering the opinion of susceptible individuals to the disease, the view of the population at baseline influences its dynamics. The results are expected to inform public policy in the context of emerging and re-emerging infectious diseases.

Novel Approach for Identification of Basic and Effective Reproduction Numbers Illustrated with COVID-19.

This paper presents a novel numerical technique for the identification of effective and basic reproduction numbers, Re and R0, for long-term epidemics, using an inverse problem approach. The method is based on the direct integration of the SIR (Susceptible-Infectious-Removed) system of ordinary differential equations and the least-squares method. Simulations were conducted using official COVID-19 data for the United States and Canada, and for the states of Georgia, Texas, and Louisiana, for a period of two years and ten months. The results demonstrate the applicability of the method in simulating the dynamics of the epidemic and reveal an interesting relationship between the number of currently infectious individuals and the effective reproduction number, which is a useful tool for predicting the epidemic dynamics. For all conducted experiments, the results show that the local maximum (and minimum) values of the time-dependent effective reproduction number occur approximately three weeks before the local maximum (and minimum) values of the number of currently infectious individuals. This work provides a novel and efficient approach for the identification of time-dependent epidemics parameters.

Dimension reduction in higher-order contagious phenomena.

We investigate epidemic spreading in a deterministic susceptible-infected-susceptible model on uncorrelated heterogeneous networks with higher-order interactions. We provide a recipe for the construction of one-dimensional reduced model (resilience function) of the N-dimensional susceptible-infected-susceptible dynamics in the presence of higher-order interactions. Utilizing this reduction process, we are able to capture the microscopic and macroscopic behavior of infectious networks. We find that the microscopic state of nodes (fraction of stable healthy individual of each node) inversely scales with their degree, and it becomes diminished due to the presence of higher-order interactions. In this case, we analytically obtain that the macroscopic state of the system (fraction of infectious or healthy population) undergoes abrupt transition. Additionally, we quantify the network's resilience, i.e., how the topological changes affect the stable infected population. Finally, we provide an alternative framework of dimension reduction based on the spectral analysis of the network, which can identify the critical onset of the disease in the presence or absence of higher-order interactions. Both reduction methods can be extended for a large class of dynamical models.

Epidemic modeling with heterogeneity and social diffusion.

We propose and analyze a family of epidemiological models that extend the classic Susceptible-Infectious-Recovered/Removed (SIR)-like framework to account for dynamic heterogeneity in infection risk. The family of models takes the form of a system of reaction-diffusion equations given populations structured by heterogeneous susceptibility to infection. These models describe the evolution of population-level macroscopic quantities S, I, R as in the classical case coupled with a microscopic variable f, giving the distribution of individual behavior in terms of exposure to contagion in the population of susceptibles. The reaction terms represent the impact of sculpting the distribution of susceptibles by the infection process. The diffusion and drift terms that appear in a Fokker-Planck type equation represent the impact of behavior change both during and in the absence of an epidemic. We first study the mathematical foundations of this system of reaction-diffusion equations and prove a number of its properties. In particular, we show that the system will converge back to the unique equilibrium distribution after an epidemic outbreak. We then derive a simpler system by seeking self-similar solutions to the reaction-diffusion equations in the case of Gaussian profiles. Notably, these self-similar solutions lead to a system of ordinary differential equations including classic SIR-like compartments and a new feature: the average risk level in the remaining susceptible population. We show that the simplified system exhibits a rich dynamical structure during epidemics, including plateaus, shoulders, rebounds and oscillations. Finally, we offer perspectives and caveats on ways that this family of models can help interpret the non-canonical dynamics of emerging infectious diseases, including COVID-19.

Air Pollution and Mortality at the Intersection of Race and Social Class.

BACKGROUND: Black Americans are exposed to higher annual levels of air pollution containing fine particulate matter (particles with an aerodynamic diameter of ≤2.5 µm [PM2.5]) than White Americans and may be more susceptible to its health effects. Low-income Americans may also be more susceptible to PM2.5 pollution than high-income Americans. Because information is lacking on exposure-response curves for PM2.5 exposure and mortality among marginalized subpopulations categorized according to both race and socioeconomic position, the Environmental Protection Agency lacks important evidence to inform its regulatory rulemaking for PM2.5 standards. METHODS: We analyzed 623 million person-years of Medicare data from 73 million persons 65 years of age or older from 2000 through 2016 to estimate associations between annual PM2.5 exposure and mortality in subpopulations defined simultaneously by racial identity (Black vs. White) and income level (Medicaid eligible vs. ineligible). RESULTS: Lower PM2.5 exposure was associated with lower mortality in the full population, but marginalized subpopulations appeared to benefit more as PM2.5 levels decreased. For example, the hazard ratio associated with decreasing PM2.5 from 12 µg per cubic meter to 8 µg per cubic meter for the White higher-income subpopulation was 0.963 (95% confidence interval [CI], 0.955 to 0.970), whereas equivalent hazard ratios for marginalized subpopulations were lower: 0.931 (95% CI, 0.909 to 0.953) for the Black higher-income subpopulation, 0.940 (95% CI, 0.931 to 0.948) for the White low-income subpopulation, and 0.939 (95% CI, 0.921 to 0.957) for the Black low-income subpopulation. CONCLUSIONS: Higher-income Black persons, low-income White persons, and low-income Black persons may benefit more from lower PM2.5 levels than higher-income White persons. These findings underscore the importance of considering racial identity and income together when assessing health inequities. (Funded by the National Institutes of Health and the Alfred P. Sloan Foundation.).