arXiv subjects

Robin N. Thompson

Publications and source records attributed to Robin N. Thompson.

4 recordsLinked to original sources

arXiv2026

Multi-scale measures of time-varying epidemic spread on human mobility networks

Human movement drives the spatial spread and persistence of many infectious diseases, yet existing theory and real-time operational tools for inferring the instantaneous reproduction number R(t) often assume static and/or homogeneously mixing populations and cannot describe how individuals generate and acquire infections heterogeneously based on their movement patterns within a day. Renewal equations underpin many such popular estimators of R(t), and here, we develop a network-based modelling framework from which we derive new mechanism-led renewal equations and control indicators for outbreaks of infectious diseases. These equations directly integrate within-day human movement to rigorously define a family of instantaneous reproduction numbers; inward, outward, and type R(t) for individual locations, R(t) between locations, R(t) at meeting locations, and R(t) for the entire mobility network. These quantities correct for the unsuitability of existing location-specific R(t) estimators that operate in closed, static populations. Applying our framework to epidemics on diverse types of networks alongside mobile phone data, we demonstrate how our new framework's outputs provide new, multi-scale control indicators at the network, location, and transmission corridor scales, and can be used to design targeted disease control interventions including the strength, type, and length of intervention required across space and time. We capture the biasing effects of different existing ways to measure location-specific and network-level transmission potential without capturing within-day human movements. This generalisable framework redefines reproduction numbers in real-world outbreaks that are shaped by individuals moving across connected locations, enabling more spatially and temporally precise interventions.

q-bio.QM↗

arXiv2026

Outbreak dynamics and population vulnerability in stochastic epidemic models on networks

During infectious disease epidemics, pathogen transmission occurs in host populations made up of interacting subpopulations. Using stochastic simulation and analytical approximations, we examine how outbreak sizes in networked populations depend on network architecture, subpopulation sizes and the strength of coupling between subpopulations. We find, as expected, that mean outbreak sizes are frequently lower in networked populations than in homogeneous populations with the same basic reproduction number. However, after an outbreak ends, a networked population is often vulnerable to further outbreaks, and the ending of an outbreak may not imply herd immunity in any sense. Another key finding is that a relatively small amount of randomly distributed prior immunity can be more protective in a networked population than a homogeneous population, a phenomenon which can be reproduced analytically in certain cases. We also find that in networked populations, randomly distributed prior immunity is often more protective than infection-acquired immunity; but this conclusion can be reversed in populations with highly variable susceptibility. All of these conclusions have implications for designing outbreak control strategies that aim to reduce pathogen transmission during epidemics.

q-bio.PE↗

arXiv2025

A primer on inference and prediction with epidemic renewal models and sequential Monte Carlo

Renewal models are widely used in statistical epidemiology as semi-mechanistic models of disease transmission. While primarily used for estimating the instantaneous reproduction number, they can also be used for generating projections, estimating elimination probabilities, modelling the effect of interventions, and more. We demonstrate how simple sequential Monte Carlo methods (also known as particle filters) can be used to perform inference on these models. Our goal is to acquaint a reader who has a working knowledge of statistical inference with these methods and models and to provide a practical guide to their implementation. We focus on these methods' flexibility and their ability to handle multiple statistical and other biases simultaneously. We leverage this flexibility to unify existing methods for estimating the instantaneous reproduction number and generating projections. A companion website SMC and epidemic renewal models provides additional worked examples, self-contained code to reproduce the examples presented here, and additional materials.

stat.ME↗

arXiv2024

Renewal equations for vector-borne diseases

During infectious disease outbreaks, estimates of time-varying pathogen transmissibility, such as the instantaneous reproduction number R(t) or epidemic growth rate r(t), are used to inform decision-making by public health authorities. For directly transmitted infectious diseases, the renewal equation framework is a widely used method for measuring time-varying transmissibility. The framework uses information on the typical time elapsing between an infection and the offspring infections (quantified by the generation time distribution), and R(t), to describe the rate at which currently infected individuals generate new infections. For diseases with transmission cycles involving hosts and vectors, however, renewal equation models have been far less used. This is likely due to difficulties in mechanistically defining generation times that can capture the complexity of multi-stage, human-vector relationships. Here, using dengue as an example, we provide general renewal equations that are derived from first principles using age-structured systems of coupled partial differential equations across human and vector sub-populations. Our framework tracks the multi-stage transmission cycle over calendar time and across stage-specific ages, resulting in governing renewal equations that quantify how the rate at which new infections are generated from existing infections depends on stage-specific processes. The framework provides a foundation on which to base inferential frameworks for estimating R(t) and r(t) for infectious diseases with multiple stages in the transmission cycle

q-bio.PE↗