Search

Susceptible-infectious-recovered-susceptible (SIRS) epidemic models assume that individual immunity wanes in one leap, from complete immunity to complete susceptibility. For many diseases immunity on the contrary wanes gradually, something that has become even more evident during COVID-19 pandemic where also recently infected have a reinfection risk, and booster vaccines are given to increase immunity. Here, a novel mathematical model is presented allowing for the gradual decay of immunity following linear or exponential waning functions. The two new models and the SIRS model are compared assuming all three models have the same cumulative immunity. When no intervention is put in place, we find that the long-term prevalence is higher for the models with gradual waning. If aiming for herd immunity by continuous vaccination, it is shown that larger vaccine quantities are required when immunity wanes gradually compared with results obtained from the SIRS model, and this difference is the biggest for the most realistic assumption of exponentially waning of immunity. For parameter choices fitting to COVID-19, the critical amount of vaccine supply is about 50% higher if immunity wanes linearly, and more than 150% higher when immunity wanes exponentially, when compared with the classic SIRS epidemic model.

A Markovian Susceptible [Formula: see text] Infectious [Formula: see text] Recovered (SIR) model is considered for the spread of an epidemic on a configuration model network, in which susceptible individuals may take preventive measures by dropping edges to infectious neighbours. An effective degree formulation of the model is used in conjunction with the theory of density dependent population processes to obtain a law of large numbers and a functional central limit theorem for the epidemic as the population size [Formula: see text], assuming that the degrees of individuals are bounded. A central limit theorem is conjectured for the final size of the epidemic. The results are obtained for both the Molloy-Reed (in which the degrees of individuals are deterministic) and Newman-Strogatz-Watts (in which the degrees of individuals are independent and identically distributed) versions of the configuration model. The two versions yield the same limiting deterministic model but the asymptotic variances in the central limit theorems are greater in the Newman-Strogatz-Watts version. The basic reproduction number [Formula: see text] and the process of susceptible individuals in the limiting deterministic model, for the model with dropping of edges, are the same as for a corresponding SIR model without dropping of edges but an increased recovery rate, though, when [Formula: see text], the probability of a major outbreak is greater in the model with dropping of edges. The results are specialised to the model without dropping of edges to yield conjectured central limit theorems for the final size of Markovian SIR epidemics on configuration-model networks, and for the size of the giant components of those networks. The theory is illustrated by numerical studies, which demonstrate that the asymptotic approximations are good, even for moderate N.

The outbreak of an infectious disease in a human population can lead to individuals responding with preventive measures in an attempt to avoid getting infected. This leads to changes in contact patterns. However, as we show in this paper, rational behaviour at the individual level, such as social distancing from infectious contacts, may not always be beneficial for the population as a whole. We use epidemic network models to demonstrate the potential negative consequences at the population level. We take into account the social structure of the population through several network models. As the epidemic evolves, susceptible individuals may distance themselves from their infectious contacts. Some individuals replace their lost social connections by seeking new ties. If social distancing occurs at a high rate at the beginning of an epidemic, then this can prevent an outbreak from occurring. However, we show that moderate social distancing can worsen the disease outcome, both in the initial phase of an outbreak and the final epidemic size. Moreover, the same negative effect can arise in real-world networks. Our results suggest that one needs to be careful when targeting behavioural changes as they could potentially worsen the epidemic outcome. Furthermore, network structure crucially influences the way that individual-level measures impact the epidemic at the population level. These findings highlight the importance of careful analysis of preventive measures in epidemic models., (© 2018 The Author(s).)

What role do asymptomatically infected individuals play in the transmission dynamics? There are many diseases, such as norovirus and influenza, where some infected hosts show symptoms of the disease while others are asymptomatically infected, i.e. do not show any symptoms. The current paper considers a class of epidemic models following an SEIR (Susceptible  →  Exposed  →  Infectious  →  Recovered) structure that allows for both symptomatic and asymptomatic cases. The following question is addressed: what fraction ρ of those individuals getting infected are infected by symptomatic (asymptomatic) cases? This is a more complicated question than the related question for the beginning of the epidemic: what fraction of the expected number of secondary cases of a typical newly infected individual, i.e. what fraction of the basic reproduction number R 0 , is caused by symptomatic individuals? The latter fraction only depends on the type-specific reproduction numbers, while the former fraction ρ also depends on timing and hence on the probabilistic distributions of latent and infectious periods of the two types (not only their means). Bounds on ρ are derived for the situation where these distributions (and even their means) are unknown. Special attention is given to the class of Markov models and the class of continuous-time Reed-Frost models as two classes of distribution functions for latent and infectious periods. We show how these two classes of models can exhibit very different behaviour., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)

An SEIRS epidemic with disease fatalities is introduced in a growing population (modelled as a super-critical linear birth and death process). The study of the initial phase of the epidemic is stochastic, while the analysis of the major outbreaks is deterministic. Depending on the values of the parameters, the following scenarios are possible. i) The disease dies out quickly, only infecting few; ii) the epidemic takes off, the number of infected individuals grows exponentially, but the fraction of infected individuals remains negligible; iii) the epidemic takes off, the number of infected grows initially quicker than the population, the disease fatalities diminish the growth rate of the population, but it remains super critical, and the fraction of infected go to an endemic equilibrium; iv) the epidemic takes off, the number of infected individuals grows initially quicker than the population, the diseases fatalities turn the exponential growth of the population to an exponential decay., (Copyright © 2017 Elsevier Inc. All rights reserved.)

This paper is concerned with stochastic SIR and SEIR epidemic models on random networks in which individuals may rewire away from infected neighbors at some rate [Formula: see text] (and reconnect to non-infectious individuals with probability [Formula: see text] or else simply drop the edge if [Formula: see text]), so-called preventive rewiring. The models are denoted SIR-[Formula: see text] and SEIR-[Formula: see text], and we focus attention on the early stages of an outbreak, where we derive the expressions for the basic reproduction number [Formula: see text] and the expected degree of the infectious nodes [Formula: see text] using two different approximation approaches. The first approach approximates the early spread of an epidemic by a branching process, whereas the second one uses pair approximation. The expressions are compared with the corresponding empirical means obtained from stochastic simulations of SIR-[Formula: see text] and SEIR-[Formula: see text] epidemics on Poisson and scale-free networks. Without rewiring of exposed nodes, the two approaches predict the same epidemic threshold and the same [Formula: see text] for both types of epidemics, the latter being very close to the mean degree obtained from simulated epidemics over Poisson networks. Above the epidemic threshold, pairwise models overestimate the value of [Formula: see text] computed from simulations, which turns out to be very close to the one predicted by the branching process approximation. When exposed individuals also rewire with [Formula: see text] (perhaps unaware of being infected), the two approaches give different epidemic thresholds, with the branching process approximation being more in agreement with simulations.

Recent work has attempted to use whole-genome sequence data from pathogens to reconstruct the transmission trees linking infectors and infectees in outbreaks. However, transmission trees from one outbreak do not generalize to future outbreaks. Reconstruction of transmission trees is most useful to public health if it leads to generalizable scientific insights about disease transmission. In a survival analysis framework, estimation of transmission parameters is based on sums or averages over the possible transmission trees. A phylogeny can increase the precision of these estimates by providing partial information about who infected whom. The leaves of the phylogeny represent sampled pathogens, which have known hosts. The interior nodes represent common ancestors of sampled pathogens, which have unknown hosts. Starting from assumptions about disease biology and epidemiologic study design, we prove that there is a one-to-one correspondence between the possible assignments of interior node hosts and the transmission trees simultaneously consistent with the phylogeny and the epidemiologic data on person, place, and time. We develop algorithms to enumerate these transmission trees and show these can be used to calculate likelihoods that incorporate both epidemiologic data and a phylogeny. A simulation study confirms that this leads to more efficient estimates of hazard ratios for infectiousness and baseline hazards of infectious contact, and we use these methods to analyze data from a foot-and-mouth disease virus outbreak in the United Kingdom in 2001. These results demonstrate the importance of data on individuals who escape infection, which is often overlooked. The combination of survival analysis and algorithms linking phylogenies to transmission trees is a rigorous but flexible statistical foundation for molecular infectious disease epidemiology.

Consider a uniformly mixing population which grows as a super-critical linear birth and death process. At some time an infectious disease (of SIR or SEIR type) is introduced by one individual being infected from outside. It is shown that three different scenarios may occur: (i) an epidemic never takes off, (ii) an epidemic gets going and grows but at a slower rate than the community thus still being negligible in terms of population fractions, or (iii) an epidemic takes off and grows quicker than the community eventually leading to an endemic equilibrium. Depending on the parameter values, either scenario (i) is the only possibility, both scenarios (i) and (ii) are possible, or scenarios (i) and (iii) are possible.

A random network model which allows for tunable, quite general forms of clustering, degree correlation and degree distribution is defined. The model is an extension of the configuration model, in which stubs (half-edges) are paired to form a network. Clustering is obtained by forming small completely connected subgroups, and positive (negative) degree correlation is obtained by connecting a fraction of the stubs with stubs of similar (dissimilar) degree. An SIR (Susceptible --> Infective --> Recovered) epidemic model is defined on this network. Asymptotic properties of both the network and the epidemic, as the population size tends to infinity, are derived: the degree distribution, degree correlation and clustering coefficient, as well as a reproduction number R(*), the probability of a major outbreak and the relative size of such an outbreak. The theory is illustrated by Monte Carlo simulations and numerical examples. The main findings are that (1) clustering tends to decrease the spread of disease, (2) the effect of degree correlation is appreciably greater when the disease is close to threshold than when it is well above threshold and (3) disease spread broadly increases with degree correlation ρ when R(*) is just above its threshold value of one and decreases with ρ when R(*) is well above one.

This paper is concerned with SIR (susceptible → infected → removed) household epidemic models in which the infection response may be either mild or severe, with the type of response also affecting the infectiousness of an individual. Two different models are analysed. In the first model, the infection status of an individual is predetermined, perhaps due to partial immunity, and in the second, the infection status of an individual depends on the infection status of its infector and on whether the individual was infected by a within- or between-household contact. The first scenario may be modelled using a multitype household epidemic model, and the second scenario by a model we denote by the infector-dependent-severity household epidemic model. Large population results of the two models are derived, with the focus being on the distribution of the total numbers of mild and severe cases in a typical household, of any given size, in the event that the epidemic becomes established. The aim of the paper is to investigate whether it is possible to determine which of the two underlying explanations is causing the varying response when given final size household outbreak data containing mild and severe cases. We conduct numerical studies which show that, given data on sufficiently many households, it is generally possible to discriminate between the two models by comparing the Kullback-Leibler divergence for the two fitted models to these data.

This paper is a survey paper on stochastic epidemic models. A simple stochastic epidemic model is defined and exact and asymptotic (relying on a large community) properties are presented. The purpose of modelling is illustrated by studying effects of vaccination and also in terms of inference procedures for important parameters, such as the basic reproduction number and the critical vaccination coverage. Several generalizations towards realism, e.g. multitype and household epidemic models, are also presented, as is a model for endemic diseases., (2010 Elsevier Inc. All rights reserved.)

Epidemic models are always simplifications of real world epidemics. Which real world features to include, and which simplifications to make, depend both on the disease of interest and on the purpose of the modelling. In the present paper we discuss some such purposes for which a stochastic model is preferable to a deterministic counterpart. The two main examples illustrate the importance of allowing the infectious and latent periods to be random when focus lies on the probability of a large epidemic outbreak and/or on the initial speed, or growth rate, of the epidemic. A consequence of the latter is that estimation of the basic reproduction number R(0) is sensitive to assumptions about the distributions of the infectious and latent periods when using data from the early stages of an outbreak, which we illustrate with data from the H1N1 influenza A pandemic. Some further examples are also discussed as are some practical consequences related to these stochastic aspects.

A stochastic epidemic model allowing for both mildly and severely infectious individuals is defined, where an individual can become severely infectious directly upon infection or if additionally exposed to infection. It is shown that, assuming a large community, the initial phase of the epidemic may be approximated by a suitable branching process and that the main part of an epidemic that becomes established admits a law of large numbers and a central limit theorem, leading to a normal approximation for the final outcome of such an epidemic. Effects of vaccination prior to an outbreak are studied and the critical vaccination coverage, above which only small outbreaks can occur, is derived. The results are illustrated by simulations that demonstrate that the branching process and normal approximations work well for finite communities, and by numerical examples showing that the final outcome may be close to discontinuous in certain model parameters and that the fraction mildly infected may actually increase as an effect of vaccination.

We consider a (social) network whose structure can be represented by a simple random graph having a pre-specified degree distribution. A Markovian susceptible-infectious-removed (SIR) epidemic model is defined on such a social graph. We then consider two real-time vaccination models for contact tracing during the early stages of an epidemic outbreak. The first model considers vaccination of each friend of an infectious individual (once identified) independently with probability p. The second model is related to the first model but also sets a bound on the maximum number an infectious individual can infect before being identified. Expressions are derived for the influence on the reproduction number of these vaccination models. We give some numerical examples and simulation results based on the Poisson and heavy-tail degree distributions where it is shown that the second vaccination model has a bigger advantage compared to the first model for the heavy-tail degree distribution.

The real-time analysis of infectious disease surveillance data is essential in obtaining situational awareness about the current dynamics of a major public health event such as the COVID-19 pandemic. This analysis of e.g., time-series of reported cases or fatalities is complicated by reporting delays that lead to under-reporting of the complete number of events for the most recent time points. This can lead to misconceptions by the interpreter, for instance the media or the public, as was the case with the time-series of reported fatalities during the COVID-19 pandemic in Sweden. Nowcasting methods provide real-time estimates of the complete number of events using the incomplete time-series of currently reported events and information about the reporting delays from the past. In this paper we propose a novel Bayesian nowcasting approach applied to COVID-19-related fatalities in Sweden. We incorporate additional information in the form of time-series of number of reported cases and ICU admissions as leading signals. We demonstrate with a retrospective evaluation that the inclusion of ICU admissions as a leading signal improved the nowcasting performance of case fatalities for COVID-19 in Sweden compared to existing methods. Author summary: Nowcasting methods are an essential tool to provide situational awareness in a pandemic. The methods aim to provide real-time estimates of the complete number of events using the incomplete time-series of currently reported events and the information about the reporting delays from the past. In this paper, we propose a Bayesian approach applied to COVID-19 fatalities in Sweden. We incorporate regression components into the Bayesian hierarchical model to accommodate additional information provided by leading indicators such as time-series of the number of reported cases and ICU admissions. We use a retrospective evaluation covering the second (alpha) and third (delta) wave of COVID-19 in Sweden to assess the performance of the proposed method. We demonstrate that the inclusion of ICU admissions as a regression component improved the nowcasting performance (measured by the CRPS score) of case fatalities for COVID-19 in Sweden by 3.9% compared to when this information was not incorporated into the model. [ABSTRACT FROM AUTHOR]

In this paper we present a family of models that allows us to estimate egos’ unobserved action dispositions from a joint behavioural outcome of a dyadic social interaction process of both egos’ and alters’ action dispositions. The method is put to test on a data set containing two different types of dyadic activities of high relevance for the spread of sexually transmitted infections (STI), condom use and anal sex. The data consists of individuals older than 15 years old who visited one of the nine youth clinics in the Vastra Gotaland region of Sweden between February 2010 and March 2011 for STI testing. This is hence a group of special interest for STI interventions. We cannot find any difference in condom disposition between women and men. Condoms are initially used more often in less risky types of relationships, especially if the partner ends up as a main partner. When studying the disposition towards anal sex we do however find a difference between men and women. Women are more against practising anal sex than men while the majority of men are neutral towards anal sex. [ABSTRACT FROM AUTHOR]

We study continuous-time birth-death type processes, where individuals have independent and identically distributed lifetimes, according to a random variable Q, with E[Q] = 1, and where the birth rate if the population is currently in state (has size) n is α(n). We focus on two important examples, namely α(n) = λn being a branching process, and α(n) = λn(N-n)/N which corresponds to an SIS (susceptible→infective →susceptible) epidemic model in a homogeneously mixing community of fixed size N. The processes are assumed to start with a single individual, i.e. in state 1. Let T , An, C, and S denote the (random) time to extinction, the total time spent in state n, the total number of individuals ever alive, and the sum of the lifetimes of all individuals in the birth-death process, respectively. We give expressions for the expectation of all these quantities and showthat these expectations are insensitive to the distribution of Q. We also derive an asymptotic expression for the expected time to extinction of the SIS epidemic, but now starting at the endemic state, which is not independent of the distribution of Q. The results are also applied to the household SIS epidemic, showing that, in contrast to the household SIR (susceptible → infective → recovered) epidemic, its threshold parameter R* is insensitive to the distribution of Q. [ABSTRACT FROM AUTHOR]

A random graph model with prescribed degree distribution and degree dependent edge weights is introduced. Each vertex is independently equipped with a random number of half-edges and each half-edge is assigned an integer valued weight according to a distribution that is allowed to depend on the degree of its vertex. Half-edges with the same weight are then paired randomly to create edges. An expression for the threshold for the appearance of a giant component in the resulting graph is derived using results on multi-type branching processes. The same technique also gives an expression for the basic reproduction number for an epidemic on the graph where the probability that a certain edge is used for transmission is a function of the edge weight (reflecting how closely 'connected' the corresponding vertices are). It is demonstrated that, if vertices with large degree tend to have large (small) weights on their edges and if the transmission probability increases with the edge weight, then it is easier (harder) for the epidemic to take off compared to a randomized epidemic with the same degree and weight distribution. A recipe for calculating the probability of a large outbreak in the epidemic and the size of such an outbreak is also given. Finally, the model is fitted to three empirical weighted networks of importance for the spread of contagious diseases and it is shown that R can be substantially over- or underestimated if the correlation between degree and weight is not taken into account. [ABSTRACT FROM AUTHOR]

We analyse a Markovian SIS epidemic amongst a finite population partitioned into households. Since the population is finite, the epidemic will eventually go extinct, i.e., have no more infectives in the population. We study the effects of population size and within household transmission upon the time to extinction. This is done through two approximations. The first approximation is suitable for all levels of within household transmission and is based upon an Ornstein-Uhlenbeck process approximation for the diseases fluctuations about an endemic level relying on a large population. The second approximation is suitable for high levels of within household transmission and approximates the number of infectious households by a simple homogeneously mixing SIS model with the households replaced by individuals. The analysis, supported by a simulation study, shows that the mean time to extinction is minimized by moderate levels of within household transmission. [ABSTRACT FROM AUTHOR]

Consider a random graph, having a prespecified degree distribution F, but other than that being uniformly distributed, describing the social structure (friendship) in a large community. Suppose that one individual in the community is externally infected by an infectious disease and that the disease has its course by assuming that infected individuals infect their not yet infected friends independently with probability p. For this situation, we determine the values of R0, the basic reproduction number, and τ0 the asymptotic final size in the case of a major outbreak. Furthermore, we examine some different local vaccination strategies, where individuals are chosen randomly and vaccinated, or friends of the selected individuals are vaccinated, prior to the introduction of the disease. For the studied vaccination strategies, we determine Rv, the reproduction number, and τv, the asymptotic final proportion infected in the case of a major outbreak, after vaccinating a fraction v. [ABSTRACT FROM AUTHOR]

Let CV and C0 denote the number of cases among vaccinated and unvaccinated individuals, respectively, and let υ be the proportion of individuals vaccinated. The quantity ê = 1–(1–υ)CV/(υC0) = 1–(relative attack rate) is the most used estimator of the effectiveness of a vaccine to protect against infection. For a wide class of vaccine responses, a family of transmission models and three types of community settings, this paper investigates what ê actually estimates. It does so under the assumption that the community is large and the vaccination coverage is adequate to prevent major outbreaks of the infectious disease, so that only data on minor outbreaks are available. For a community of homogeneous individuals who mix uniformly, it is found that ê estimates a quantity with the interpretation of 1–(mean susceptibility, per contact, of vaccinees relative to unvaccinated individuals). We provide a standard error for ê in this setting. For a community with some heterogeneity ê can be a very misleading estimator of the effectiveness of the vaccine. When individuals have inherent differences, ê estimates a quantity that depends also on the inherent susceptibilities of different types of individual and on the vaccination coverage for different types. For a community of households, ê estimates a quantity that depends on the rate of transmission within households and on the reduction in infectivity induced by the vaccine. In communities that are structured, into households or age‐groups, it is possible that ê estimates a value that is negative even when the vaccine reduces both susceptibility and infectivity. [ABSTRACT FROM AUTHOR]

A stochastic multitype model for the spread of an infectious disease in a community of heterogeneous individuals is analysed. In particular, estimates of R [sub 0] (the basic reproduction number) and the critical vaccination coverage are derived, where estimation is based on final size data of an outbreak in the community. It is shown that these key parameters cannot be estimated consistently from data; only upper and lower bounds can be estimated. Confidence regions for the upper bounds are derived, thus giving conservative estimates of R [sub 0] and the fractions necessary to vaccinate. [ABSTRACT FROM AUTHOR]