arXiv subjects

Tom Britton

Publications and source records attributed to Tom Britton.

At least 37 records · Page 2Linked to original sources

arXiv2020

The disease-induced herd immunity level for Covid-19 is substantially lower than the classical herd immunity level

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.

q-bio.PE↗

arXiv2020

Stochastic epidemics in a homogeneous community

These notes describe stochastic epidemics in a homogenous community. Our main concern is stochastic compartmental models (i.e. models where each individual belongs to a compartment, which stands for its status regarding the epidemic under study : S for susceptible, E for exposed, I for infectious, R for recovered) for the spread of an infectious disease. In the present notes we restrict ourselves to homogeneously mixed communities. We present our general model and study the early stage of the epidemic in chapter 1. Chapter 2 studies the particular case of Markov models, especially in the asymptotic of a large population, which leads to a law of large numbers and a central limit theorem. Chapter 3 considers the case of a closed population, and describes the final size of the epidemic (i.e. the total number of individuals who ever get infected). Chapter 4 considers models with a constant influx of susceptibles (either by birth, immigration of loss of immunity of recovered individuals), and exploits the CLT and Large Deviations to study how long it takes for the stochastic disturbances to stop an endemic situation which is stable for the deterministic epidemic model. The document ends with an Appendix which presents several mathematical notions which are used in these notes, as well as solutions to many of the exercises which are proposed in the various chapters.

math.PR↗

arXiv2019

Epidemic models on social networks -- with inference

Consider stochastic models for the spread of an infection in a structured community, where this structured community is itself described by a random network model. Some common network models and transmission models are defined and large population proporties of them are presented. Focus is then shifted to statistical methodology: what can be estimated and how, depending on the underlying network, transmission model and the available data? This survey paper discusses several different scenarios, also giving references to publications where more details can be found.

q-bio.PE↗

arXiv2019

A stochastic SIR network epidemic model with preventive dropping of edges

A Markovian SIR (Susceptible-Infectious-Recovered) 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 $N \to \infty$, 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 theorema are greater in the Newman-Strogatz-Watts version. The basic reproduction number $R_0$ 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 $R_0>1$, 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 giant components of those networks. The theory is illustrated by numerical studies, which demonstrate that the asymptotic approximations are good, even for moderate $N$.

math.PR↗

arXiv2018

Directed preferential attachment models

The directed preferential attachment model is revisited. A new exact characterization of the limiting in- and out-degree distribution is given by two \emph{independent} pure birth processes that are observed at a common exponentially distributed time $T$ (thus creating dependence between in- and out-degree). The characterization gives an explicit form for the joint degree distribution, and this confirms previously derived tail probabilities for the two marginal degree distributions. The new characterization is also used to obtain an explicit expression for tail probabilities in which both degrees are large. A new generalised directed prefererantial attachment model is then defined and analysed using similar methods. The two extensions, motivated by empirical evidence, are to allow double-directed (i.e.\ undirected) edges in the network, and to allow the probability to connect an ingoing (outgoing) edge to a specified node to also depend on the out-degree (in-degree) of that node.

math.PR↗

arXiv2018

Individual preventive measures during an epidemic may have negative population-level outcomes

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. We show that 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.

q-bio.PE↗

arXiv2018

Estimation in emerging epidemics: biases and remedies

When analysing new emerging infectious disease outbreaks one typically has observational data over a limited period of time and several parameters to estimate, such as growth rate, R0, serial or generation interval distribution, latent and incubation times or case fatality rates. Also parameters describing the temporal relations between appearance of symptoms, notification, death and recovery/discharge will be of interest. These parameters form the basis for predicting the future outbreak, planning preventive measures and monitoring the progress of the disease. We study the problem of making inference during the emerging phase of an outbreak and point out potential sources of bias related to contact tracing, replacing generation times by serial intervals, multiple potential infectors or truncation effects amplified by exponential growth. These biases directly affect the estimation of e.g. the generation time distribution and the case fatality rate, but can then propagate to other estimates, e.g. of R0 and growth rate. Many of the traditionally used estimation methods in disease epidemiology may suffer from these biases when applied to the emerging disease outbreak situation. We show how to avoid these biases based on proper statistical modelling. We illustrate the theory by numerical examples and simulations based on the recent 2014-15 Ebola outbreak to quantify possible estimation biases, which may be up to 20% underestimation of R0, if the epidemic growth rate is fitted to observed data or, conversely, up to 62% overestimation of the growth rate if the correct R0 is used in conjunction with the Euler-Lotka equation.

stat.AP↗

arXiv2018

Basic stochastic transmission models and their inference

The current survey paper concerns stochastic mathematical models for the spread of infectious diseases. It starts with the simplest setting of a homogeneous population in which a transmittable disease spreads during a short outbreak. Assuming a large population some important features are presented: branching process approximation, basic reproduction number $R_0$, and final size of an outbreak. Some extensions towards realism are then discussed: models for endemicity, various heterogeneities, and prior immmunity. The focus is then shifted to statistical inference. What can be estimated for these models for various levels of detailed data and with what precision? The paper ends by describing how the inference results may be used for determining successful vaccination strategies. This paper will appear as a chapter of a forthcoming book entitled \emph{Handbook of Infectious Disease Epidemiology}.

stat.AP↗

arXiv2018

Who is the infector? General multi-type epidemics and real-time susceptibility processes

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.

math.PR↗

arXiv2018

Who is the infector? Epidemic models with symptomatic and asymptomatic cases

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 $\to$ Exposed $\to$ Infectious $\to$ 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. We show how these two classes of models can exhibit very different behaviour.

q-bio.PE↗

arXiv2017

A spatial epidemic model with site contamination

We introduce the effect of site contamination in a model for spatial epidemic spread and show that the presence of site contamination may have a strict effect on the model in the sense that it can make an otherwise subcritical process supercritical. Each site on $\mathbb{Z}^d$ is independently assigned a random number of particles and these then perform random walks restricted to bounded regions around their home locations. At time 0, the origin is infected along with all its particles. The infection then spread in that an infected particle that jumps to a new site causes the site along with all particles located there to be infected. Also, a healthy particle that jumps to a site where infection is presents, either in that the site is infected or in the presence of infected particles, becomes infected. Particles and sites recover at rate $λ$ and $γ$, respectively, and then become susceptible to the infection again. We show that, for each given value of $λ$, there is a positive probability that the infection survives indefinitely if $γ$ is sufficiently small, and that, for each given value of $γ$, the infection dies out almost surely if $λ$ is large enough. Several open problems and modifications of the model are discussed, and some natural conjectures are supported by simulations.

math.PR↗

arXiv2017

SEIRS epidemics in growing populations

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 \textit{number} of infected individuals grows exponentially, but the \textit{fraction} of infected individuals remains negligible; iii) the epidemic takes off, the \textit{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 \emph{fraction} of infected go to an endemic equilibrium; iv) the epidemic takes off, the \textit{number} of infected individuals grows initially quicker than the population, the diseases fatalities turn the exponential growth of the population to an exponential decay.

q-bio.PE↗

arXiv2016

A network epidemic model with preventive rewiring: comparative analysis of the initial phase

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 $ω$ (and reconnect to non-infectious individuals with probability $α$ or else simply drop the edge if $α=0$), so-called preventive rewiring. The models are denoted SIR-$ω$ and SEIR-$ω$, and we focus attention on the early stages of an outbreak, where we derive expression for the basic reproduction number $R_0$ and the expected degree of the infectious nodes $E(D_I)$ 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-$ω$ and SEIR-$ω$ epidemics on Poisson and scale-free networks. Without rewiring of exposed nodes, the two approaches predict the same epidemic threshold and the same $E(D_I)$ 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 $R_0$ 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 $α> 0$ (perhaps unaware of being infected), the two approaches give different epidemic thresholds, with the branching process approximation being more in agreement with simulations.

q-bio.PE↗

arXiv2016

Inferring $R_0$ in emerging epidemics - the effect of common population structure is small

When controlling an emerging outbreak of an infectious disease it is essential to know the key epidemiological parameters, such as the basic reproduction number $R_0$ and the control effort required to prevent a large outbreak. These parameters are estimated from the observed incidence of new cases and information about the infectious contact structures of the population in which the disease spreads. However, the relevant infectious contact structures for new, emerging infections are often unknown or hard to obtain. Here we show that for many common true underlying heterogeneous contact structures, the simplification to neglect such structures and instead assume that all contacts are made homogeneously in the whole population, results in conservative estimates for $R_0$ and the required control effort. This means that robust control policies can be planned during the early stages of an outbreak, using such conservative estimates of the required control effort.

q-bio.PE↗

arXiv2016

Molecular Infectious Disease Epidemiology: Survival Analysis and Algorithms Linking Phylogenies to Transmission Trees

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.

q-bio.QM↗

arXiv2015

Generating simple random graphs with prescribed degree distribution

Let $F$ be a probability distribution with support on the non-negative integers. Four methods for generating a simple undirected graph with (approximate) degree distribution $F$ are described and compared. Two methods are based on the so called configuration model with modifications ensuring a simple graph, one method is an extension of the classical Erdős-Rényi graph where the edge probabilities are random variables, and the last method starts with a directed random graph which is then modified to a simple undirected graph. All methods are shown to give the correct distribution in the limit of large graph size, but under different assumptions on the degree distribution $F$ and also using different order of operations.

math.PR↗

arXiv2015

An epidemic in a dynamic population with importation of infectives

Consider a large uniformly mixing dynamic population, which has constant birth rate and exponentially distributed lifetimes, with mean population size $n$. A Markovian SIR (susceptible $\to$ infective $\to$ recovered) infectious disease, having importation of infectives, taking place in this population is analysed. The main situation treated is where $n\to\infty$, keeping the basic reproduction number $R_0$ as well as the importation rate of infectives fixed, but assuming that the quotient of the average infectious period and the average lifetime tends to 0 faster than $1/\log n$. It is shown that, as $ n \to \infty$, the behaviour of the 3-dimensional process describing the evolution of the fraction of the population that are susceptible, infective and recovered, is encapsulated in a 1-dimensional regenerative process $S=\{ S(t);t\ge 0\}$ describing the limiting fraction of the population that are susceptible. The process $S$ grows deterministically, except at one random time point per regenerative cycle, where it jumps down by a size that is completely determined by the waiting time since the previous jump. Properties of the process $S$, including the jump size and stationary distributions, are determined.

math.PR↗

arXiv2015

The Configuration Model for Partially Directed Graphs

The configuration model was originally defined for undirected networks and has recently been extended to directed networks. Many empirical networks are however neither undirected nor completely directed, but instead usually partially directed meaning that certain edges are directed and others are undirected. In the paper we define a configuration model for such networks where nodes have in-, out-, and undirected degrees that may be dependent. We prove conditions under which the resulting degree distributions converge to the intended degree distributions. The new model is shown to better approximate several empirical networks compared to undirected and completely directed networks.

math.PR↗