We prove that the stationary and worst-case expected meeting times of two independent continuous-time random walks on the largest component of the Erdős-Rényi random graph G(n,p) have order n throughout the strictly supercritical, the slightly supercritical and the critical regimes. Using these bounds along with a fine-tuned combination of comparison inequalities due to Oliveira (2012) and Kanade-Mallmann-Trenn-Sauerwald (KMS, 2023), we deduce that expected coalescence time and full voter-model consensus also have order n throughout these three regimes.

We present a stochastic model for two successive SIR (Susceptible → Infectious → Recovered) epidemics in the same network structured population. Individuals infected during the first epidemic might have (partial) immunity for the second one. The first epidemic is analysed through a bond percolation model, while the second epidemic is approximated by a three-type branching process in which the types of individuals depend on their position in the percolation clusters used for the first epidemic. This branching process approximation enables us to calculate, in the large population limit and conditional upon a large outbreak in the first epidemic, a threshold parameter and the probability of a large outbreak for the second epidemic. A second branching process approximation enables us to calculate the fraction of the population that are infected by such a second large outbreak. We illustrate our results through some specific cases which have appeared previously in the literature and show that our asymptotic results give good approximations for finite populations.

We investigate final outcome properties of an SIR (susceptible -k infective -k recovered) epidemic model defined on a population of large subcommunities in which there is stronger disease transmission within the communities than between them. Our analysis involves approximation of the epidemic process by a chain of within-community large outbreaks spreading between the communities. We derive law of large numbers and central limit type results for the number of individuals and the number of communities affected and the so-called severity of the outbreak. These results are valid as the size of communities tends to infinity, with the number of communities either fixed or also tending to infinity. The weaker between-community connections lead to randomness even in the law of large numbers type limit. As part of our proofs we also obtain a new result concerning the rate of convergence of the expected fraction infected in a standard SIR epidemic to its large-population limit.

Since the beginning of the COVID-19 pandemic, the reproduction number R has become a popular epidemiological metric used to communicate the state of the epidemic. At its most basic, R is defined as the average number of secondary infections caused by one primary infected individual. R seems convenient, because the epidemic is expanding if R > 1 and contracting if R < 1 . The magnitude of R indicates by how much transmission needs to be reduced to control the epidemic. Using R in a naïve way can cause new problems. The reasons for this are threefold: (1) There is not just one definition of R but many, and the precise definition of R affects both its estimated value and how it should be interpreted. (2) Even with a particular clearly defined R , there may be different statistical methods used to estimate its value, and the choice of method will affect the estimate. (3) The availability and type of data used to estimate R vary, and it is not always clear what data should be included in the estimation. In this review, we discuss when R is useful, when it may be of use but needs to be interpreted with care, and when it may be an inappropriate indicator of the progress of the epidemic. We also argue that careful definition of R , and the data and methods used to estimate it, can make R a more useful metric for future management of the epidemic. Keywords Reproduction number , COVID-19 pandemic

New disease challenges, societal demands and better or novel types of data, drive innovations in the structure, formulation and analysis of epidemic models. Innovations in modelling can lead to new insights into epidemic processes and better use of available data, yielding improved disease control and stimulating collection of better data and new data types. Here we identify key challenges for the structure, formulation, analysis and use of mathematical models of pathogen transmission relevant to current and future pandemics.

Since the beginning of the COVID-19 pandemic, the reproduction number [Formula: see text] has become a popular epidemiological metric used to communicate the state of the epidemic. At its most basic, [Formula: see text] is defined as the average number of secondary infections caused by one primary infected individual. [Formula: see text] seems convenient, because the epidemic is expanding if [Formula: see text] and contracting if [Formula: see text]. The magnitude of [Formula: see text] indicates by how much transmission needs to be reduced to control the epidemic. Using [Formula: see text] in a naïve way can cause new problems. The reasons for this are threefold: (1) There is not just one definition of [Formula: see text] but many, and the precise definition of [Formula: see text] affects both its estimated value and how it should be interpreted. (2) Even with a particular clearly defined [Formula: see text], there may be different statistical methods used to estimate its value, and the choice of method will affect the estimate. (3) The availability and type of data used to estimate [Formula: see text] vary, and it is not always clear what data should be included in the estimation. In this review, we discuss when [Formula: see text] is useful, when it may be of use but needs to be interpreted with care, and when it may be an inappropriate indicator of the progress of the epidemic. We also argue that careful definition of [Formula: see text], and the data and methods used to estimate it, can make [Formula: see text] a more useful metric for future management of the epidemic.

We consider the spread of a supercritical stochastic SIR (Susceptible, Infectious, Recovered) epidemic on a configuration model random graph. We mainly focus on the final stages of a large outbreak and provide limit results for the duration of the entire epidemic, while we allow for non-exponential distributions of the infectious period and for both finite and infinite variance of the asymptotic degree distribution in the graph. Our analysis relies on the analysis of some subcritical continuous time branching processes and on ideas from first passage percolation. As an application we investigate the effect of vaccination with an all-or-nothing vaccine on the duration of the epidemic. We show that if vaccination fails to prevent the epidemic, it often – but not always – increases the duration of the epidemic.

We consider two classes of random graphs: (a) Poissonian random graphs in which the n vertices in the graph have i.i.d. weights distributed as X, where E(X) = μ. Edges are added according to a product measure and the probability that a vertex of weight x shares and edge with a vertex of weight y is given by 1− e−xy/(μn). (b) A thinned configuration model in which we create a ground-graph in which the n vertices have i.i.d. ground-degrees, distributed as D, with E(D) = μ. The graph of interest is obtained by deleting edges independently with probability 1− p. In both models the fraction of vertices in the largest connected component converges in probability to a constant 1 − q, where q depends on X or D and p. We investigate for which distributions X and D with given μ and p, 1−q is maximized. We show that in the class of Poissonian random graphs, X should have all its mass at 0 and one other real, which can be explicitly determined. For the thinned configuration model D should have all its mass at 0 and two subsequent positive integers.

The COVID-19 pandemic has hit different regions differently. The current disease-induced immunity level î in a region approximately equals the cumulative fraction infected, which primarily depends on two factors: (i) the initial potential for COVID-19 in the region ( R 0 ), and (ii) the preventive measures put in place. Using a mathematical model including heterogeneities owing to age, social activity and susceptibility, and allowing for time-varying preventive measures, the risk for a new epidemic wave and its doubling time are investigated. Focus lies on quantifying the minimal overall effect of preventive measures p Min needed to prevent a future outbreak. It is shown that î plays a more influential roll than when immunity is obtained from vaccination. Secondly, by comparing regions with different R 0 and î it is shown that regions with lower R 0 and low î may need higher preventive measures ( p Min ) compared with regions having higher R 0 but also higher î , even when such immunity levels are far from herd immunity. Our results are illustrated on different regions but these comparisons contain lots of uncertainty due to simplistic model assumptions and insufficient data fitting, and should accordingly be interpreted with caution.

We consider the spread of a supercritical stochastic SIR (Susceptible, Infectious, Recovered) epidemic on a configuration model random graph. We mainly focus on the final stages of a large outbreak and provide limit results for the duration of the entire epidemic, while we allow for non-exponential distributions of the infectious period and for both finite and infinite variance of the asymptotic degree distribution in the graph. Our analysis relies on the analysis of some subcritical continuous time branching processes and on ideas from first passage percolation. As an application we investigate the effect of vaccination with an all-or-nothing vaccine on the duration of the epidemic. We show that if vaccination fails to prevent the epidemic, it often – but not always – increases the duration of the epidemic.

Reviewers find that this study presents important concepts surrounding heterogeneous transmission rates and their effects on herd immunity thresholds, but suggest that there are major flaws in the modeling assumptions that produce misleading results.

Combinations of intense non-pharmaceutical interventions (lockdowns) were introduced worldwide to reduce SARS-CoV-2 transmission. Many governments have begun to implement exit strategies that relax restrictions while attempting to control the risk of a surge in cases. Mathematical modelling has played a central role in guiding interventions, but the challenge of designing optimal exit strategies in the face of ongoing transmission is unprecedented. Here, we report discussions from the Isaac Newton Institute ‘Models for an exit strategy’ workshop (11–15 May 2020). A diverse community of modellers who are providing evidence to governments worldwide were asked to identify the main questions that, if answered, would allow for more accurate predictions of the effects of different exit strategies. Based on these questions, we propose a roadmap to facilitate the development of reliable models to guide exit strategies. This roadmap requires a global collaborative effort from the scientific community and policymakers, and has three parts: (i) improve estimation of key epidemiological parameters; (ii) understand sources of heterogeneity in populations; and (iii) focus on requirements for data collection, particularly in low-to-middle-income countries. This will provide important information for planning exit strategies that balance socio-economic benefits with public health.

Most countries are suffering severely from the ongoing covid-19 pandemic despite various levels of preventive measures. A common question is if and when a country or region will reach herd immunity $h$. The classical herd immunity level $h_C$ is defined as $h_C=1-1/R_0$, where $R_0$ is the basic reproduction number, for covid-19 estimated to lie somewhere in the range 2.2-3.5 depending on country and region. It is shown here that the disease-induced herd immunity level $h_D$, after an outbreak has taken place in a country/region with a set of preventive measures put in place, is actually substantially smaller than $h_C$. As an illustration we show that if $R_0=2.5$ in an age-structured community with mixing rates fitted to social activity studies, and also categorizing individuals into three categories: low active, average active and high active, and where preventive measures affect all mixing rates proportionally, then the disease-induced herd immunity level is $h_D=43\%$ rather than $h_C=1-1/2.5=60\%$. Consequently, a lower fraction infected is required for herd immunity to appear. The underlying reason is that when immunity is induced by disease spreading, the proportion infected in groups with high contact rates is greater than that in groups with low contact rates. Consequently, disease-induced immunity is stronger than when immunity is uniformly distributed in the community as in the classical herd immunity level.

Despite various levels of preventive measures, in 2020, many countries have suffered severely from the coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. Using a model, we show that population heterogeneity can affect disease-induced immunity considerably because the proportion of infected individuals in groups with the highest contact rates is greater than that in groups with low contact rates. We estimate that if R 0 = 2.5 in an age-structured community with mixing rates fitted to social activity, then the disease-induced herd immunity level can be ~43%, which is substantially less than the classical herd immunity level of 60% obtained through homogeneous immunization of the population. Our estimates should be interpreted as an illustration of how population heterogeneity affects herd immunity rather than as an exact value or even a best estimate.

The COVID-19 pandemic has hit different parts of the world differently: some regions are still in the rise of the first wave, other regions are now facing a decline after a first wave, and yet other regions have started to see a second wave. The current immunity level î in a region is closely related to the cumulative fraction infected, which primarily depends on two factors: a) the initial potential for COVID-19 in the region (often quantified by the basic reproduction number R_0), and b) the timing, amount and effectiveness of preventive measures put in place. By means of a mathematical model including heterogeneities owing to age, social activity and susceptibility, and allowing for time-varying preventive measures, the risk for a new epidemic wave and its doubling time, and how they depend on R_0, î and the overall effect of the current preventive measures, are investigated. Focus lies on quantifying the minimal overall effect of preventive measures p_Min needed to prevent a future outbreak. The first result shows that the current immunity level î plays a more influential roll than when immunity is obtained from vaccination. Secondly, by comparing regions with different R_0 and î it is shown that regions with lower R_0 and low î may now need higher preventive measures (p_Min) compared with other regions having higher R_0 but also higher î, even when such immunity levels are far from herd immunity.

In this paper we consider SIR epidemics on random graphs with clustering. To incorporate group structure of the underlying social network, we use a generalized version of the configuration model in which each node is a member of a specified number of triangles. SIR epidemics on this type of graph have earlier been investigated under the assumption of homogeneous infectivity and also under the assumption of Poisson transmission and recovery rates. We extend known results from literature by relaxing the assumption of homogeneous infectivity. An important special case of the epidemic model analyzed in this paper is epidemics in continuous time with arbitrary infectious period distribution. We use branching process approximations of the spread of the disease to provide expressions for the basic reproduction number R0, the probability of a major outbreak and the expected final size. In addition, the impact of random vaccination with a perfect vaccine on the final outcome of the epidemic is investigated. We find that, for this particular model, R0 equals the perfect vaccine-associated reproduction number. Generalizations to groups larger than three are discussed briefly.

We couple a multi-type stochastic epidemic process with a directed random graph, where edges have random lengths. This random graph representation is used to characterise the fractions of individuals infected by the different types of vertices among all infected individuals in the large population limit. For this characterisation we rely on theory of multi-type real-time branching processes. We identify a special case of the two-type model, in which the fraction of individuals of a certain type infected by individuals of the same type, is maximised among all two-type epidemics approximated by branching processes with the same mean offspring matrix.

In this article we introduce a dynamic Erdős-Rényi graph model, in which, independently for each vertex pair, edges appear and disappear according to a Markov on-off process. In studying the dynamic graph we present two main results. The first being on how long it takes for the graph to reach stationarity. We give an explicit expression for this time, as well as proving that this is the fastest time to reach stationarity among all strong stationary times. The second result concerns the time it takes for the dynamic graph to reach a certain number of edges. We give an explicit expression for the expected value of such a time, as well as study its asymptotic behavior. This time is related to the first time the dynamic Erdős-Rényi graph contains a cluster exceeding a certain size.