arXiv subjects

Pieter Trapman

Publications and source records attributed to Pieter Trapman.

At least 19 recordsLinked to original sources

arXiv2026

Meeting and coalescence times for random walks in the largest component of the Erd\H{o}s-R\'enyi random graph

We prove that the stationary and worst-case expected meeting times of two independent continuous-time random walks on the largest component of the Erd\H{o}s-R\'enyi 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.

math.PR↗

arXiv2024

Modelling the spread of two successive SIR epidemics on a configuration model network

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.

q-bio.PE↗

arXiv2024

SIR epidemics in populations with large sub-communities

We investigate final outcome properties of an SIR (susceptible $\to$ infective $\to$ recovered) epidemic model defined on a population of large sub-communities 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.

math.PR↗

arXiv2024

Possible counter-intuitive impact of local vaccine mandates for vaccine-preventable infectious diseases

We model the impact of local vaccine mandates on the spread of vaccine-preventable infectious diseases, which in the absence of vaccines will mainly affect children. Examples of such diseases are measles, rubella, mumps and pertussis. To model the spread of the pathogen, we use a stochastic SIR (Susceptible, Infectious, Recovered) model with two levels of mixing in a closed population, often referred to as the household model. In this model individuals make local contacts within a specific small subgroup of the population (e.g.\ within a household or a school class), while they also make global contacts with random people in the population at a much lower rate than the rate of local contacts. We consider what happens if schools are given freedom to impose vaccine mandates on all of their pupils, except for the pupils that are exempt from vaccination because of medical reasons. We investigate how such a mandate affects the probability of an outbreak of a disease and the probability that a pupil that is medically exempt from vaccination, gets infected during an outbreak. We show that if the population vaccine coverage is close to the herd-immunity level then both probabilities may increase if local vaccine mandates are implemented. This is caused by unvaccinated pupils moving to schools without mandates.

physics.soc-ph↗

arXiv2020

The risk for a new COVID-19 wave -- and how it depends on $R_0$, the current immunity level and current restrictions

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 $\hat i$ 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 $R_0$, $\hat i$ 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 $\hat i$ plays a more influential roll than when immunity is obtained from vaccination. Secondly, by comparing regions with different $R_0$ and $\hat i$ it is shown that regions with lower $R_0$ and low $\hat i$ may now need higher preventive measures ($p_{Min}$) compared with other regions having higher $R_0$ but also higher $\hat i$, even when such immunity levels are far from herd immunity.

q-bio.PE↗

arXiv2020

Key Questions for Modelling COVID-19 Exit Strategies

Combinations of intense non-pharmaceutical interventions ('lockdowns') were introduced in countries worldwide to reduce SARS-CoV-2 transmission. Many governments have begun to implement lockdown exit strategies that allow restrictions to be relaxed 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, will 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. The roadmap requires a global collaborative effort from the scientific community and policy-makers, and is made up of three parts: i) improve estimation of key epidemiological parameters; ii) understand sources of heterogeneity in populations; 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.

q-bio.OT↗

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

The duration of an $SIR$ epidemic on a configuration model

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.

math.PR↗

arXiv2018

The tail does not determine the size of the giant

The size of the giant component in the configuration model, measured by the asymptotic fraction of vertices in the component, is given by a well-known expression involving the generating function of the degree distribution. In this note, we argue that the distribution over small degrees is more important for the size of the giant component than the precise distribution over very large degrees. In particular, the tail behavior of the degree distribution does not play the same crucial role for the size of the giant as it does for many other properties of the graph. Upper and lower bounds for the component size are derived for an arbitrary given distribution over small degrees $d\leq L$ and given expected degree, and numerical implementations show that these bounds are close already for small values of $L$. On the other hand, examples illustrate that, for a fixed degree tail, the component size can vary substantially depending on the distribution over small degrees.

math.PR↗

arXiv2018

SIR epidemics and vaccination on random graphs with clustering

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.

math.PR↗

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

Characterizing the Initial Phase of Epidemic Growth on some Empirical Networks

A key parameter in models for the spread of infectious diseases is the basic reproduction number $R_0$, which is the expected number of secondary cases a typical infected primary case infects during its infectious period in a large mostly susceptible population. In order for this quantity to be meaningful, the initial expected growth of the number of infectious individuals in the large-population limit should be exponential. We investigate to what extent this assumption is valid by performing repeated simulations of epidemics on selected empirical networks, viewing each epidemic as a random process in discrete time. The initial phase of each epidemic is analyzed by fitting the number of infected people at each time step to a generalised growth model, allowing for estimating the shape of the growth. For reference, similar investigations are done on some elementary graphs such as integer lattices in different dimensions and configuration model graphs, for which the early epidemic behaviour is known. We find that for the empirical networks tested in this paper, exponential growth characterizes the early stages of the epidemic, except when the network is restricted by a strong low-dimensional spacial constraint, such as is the case for the two-dimensional square lattice. However, on finite integer lattices of sufficiently high dimension, the early development of epidemics shows exponential growth.

q-bio.PE↗

arXiv2016

A Dynamic Erdős-Rényi Graph Model

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.

math.PR↗

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↗

arXiv2015

Reproduction numbers for epidemic models with households and other social structures II: comparisons and implications for vaccination

In this paper we consider epidemic models of directly transmissible SIR (susceptible $\to$ infective $\to$ recovered) and SEIR (with an additional latent class) infections in fully-susceptible populations with a social structure, consisting either of households or of households and workplaces. We review most reproduction numbers defined in the literature for these models, including the basic reproduction number $R_0$ introduced in the companion paper of this, for which we provide a simpler, more elegant derivation. Extending previous work, we provide a complete overview of the inequalities among these reproduction numbers and resolve some open questions. Special focus is put on the exponential-growth-associated reproduction number $R_r$, which is loosely defined as the estimate of $R_0$ based on the observed exponential growth of an emerging epidemic obtained when the social structure is ignored. We show that for the vast majority of the models considered in the literature $R_r \geq R_0$ when $R_0 \ge 1$ and $R_r \leq R_0$ when $R_0 \le 1$. We show that, in contrast to models without social structure, vaccination of a fraction $1-1/R_0$ of the population, chosen uniformly at random, with a perfect vaccine is usually insufficient to prevent large epidemics. In addition, we provide significantly sharper bounds than the existing ones for bracketing the critical vaccination coverage between two analytically tractable quantities, which we illustrate by means of extensive numerical examples.

q-bio.PE↗

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

Stochastic SIR epidemics in a population with households and schools

We study the spread of stochastic SIR (Susceptible $\to$ Infectious $\to$ Recovered) epidemics in two types of structured populations, both consisting of schools and households. In each of the types, every individual is part of one school and one household. In the independent partition model, the partitions of the population into schools and households are independent of each other. This model corresponds to the well-studied household-workplace model. In the hierarchical model which we introduce here, members of the same household are also members of the same school. We introduce computable branching process approximations for both types of populations and use these to compare the probabilities of a large outbreak. The branching process approximation in the hierarchical model is novel and of independent interest. We prove by a coupling argument that if all households and schools have the same size, an epidemic spreads easier (in the sense that the number of individuals infected is stochastically larger) in the independent partition model. We also show by example that this result does not necessarily hold if households and/or schools do not all have the same size.

physics.soc-ph↗