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Emerging evidence suggests that contact tracing has had limited success in the UK in reducing the R number across the COVID-19 pandemic. We investigate potential pitfalls and areas for improvement by extending an existing branching process contact tracing model, adding diagnostic testing and refining parameter estimates. Our results demonstrate that reporting and adherence are the most important predictors of programme impact but tracing coverage and speed plus diagnostic sensitivity also play an important role. We conclude that well-implemented contact tracing could bring small but potentially important benefits to controlling and preventing outbreaks, providing up to a 15% reduction in R. We reaffirm that contact tracing is not currently appropriate as the sole control measure.

Background The COVID-19 epidemic has differentially impacted communities across England, with regional variation in rates of confirmed cases, hospitalisations and deaths. Measurement of this burden changed substantially over the first months, as surveillance was expanded to accommodate the escalating epidemic. Laboratory confirmation was initially restricted to clinical need (“pillar 1”) before expanding to community-wide symptomatics (“pillar 2”). This study aimed to ascertain whether inconsistent measurement of case data resulting from varying testing coverage could be reconciled by drawing inference from COVID-19-related deaths. Methods We fit a Bayesian spatio-temporal model to weekly COVID-19-related deaths per local authority (LTLA) throughout the first wave (1 January 2020–30 June 2020), adjusting for the local epidemic timing and the age, deprivation and ethnic composition of its population. We combined predictions from this model with case data under community-wide, symptomatic testing and infection prevalence estimates from the ONS infection survey, to infer the likely trajectory of infections implied by the deaths in each LTLA. Results A model including temporally- and spatially-correlated random effects was found to best accommodate the observed variation in COVID-19-related deaths, after accounting for local population characteristics. Predicted case counts under community-wide symptomatic testing suggest a total of 275,000–420,000 cases over the first wave - a median of over 100,000 additional to the total confirmed in practice under varying testing coverage. This translates to a peak incidence of around 200,000 total infections per week across England. The extent to which estimated total infections are reflected in confirmed case counts was found to vary substantially across LTLAs, ranging from 7% in Leicester to 96% in Gloucester with a median of 23%. Conclusions Limitations in testing capacity biased the observed trajectory of COVID-19 infections throughout the first wave. Basing inference on COVID-19-related mortality and higher-coverage testing later in the time period, we could explore the extent of this bias more explicitly. Evidence points towards substantial under-representation of initial growth and peak magnitude of infections nationally, to which different parts of the country contribute unequally. ESN and GFM are funded by the Bill and Melinda Gates Foundation (ESN: OPP1183986, GFM: OPP1184344). OJB and SA are funded by the Wellcome Trust (OJB: 206471/Z/17/Z, SA: 210758/Z/18/Z, TWR: 206250/Z/17/Z). RL is funded by the Royal Society (Dorothy Hodgkin Fellowship). The following funding sources are acknowledged as providing funding for the CMMID Covid-19 working group: This research was partly funded by the Bill & Melinda Gates Foundation (OPP1183986: ESN). This research was partly funded by the Global Challenges Research Fund (GCRF) project ‘RECAP’ managed through RCUK and ESRC (ES/P010873/1: TJ). This research was partly funded by the National Institute for Health Research (NIHR) using UK aid from the UK Government to support global health research. The views expressed in this publication are those of the author(s) and not necessarily those of the NIHR or the UK Department of Health and Social Care (Health Protection Research Unit for Modelling Methodology HPRU-2012-10096: TJ). UK MRC (LID DTP MR/N013638/1: QJL; MC_PC_19065: TJ). Authors of this research receive funding from UK Public Health Rapid Support Team funded by the United Kingdom Department of Health and Social Care (TJ). Wellcome Trust (210758/Z/18/Z: SA). The following funding sources are acknowledged as providing funding for the working group authors. Alan Turing Institute (AE). BBSRC LIDP (BB/M009513/1: DS). This research was partly funded by the Bill & Melinda Gates Foundation (INV-003174: KP, MJ, YL; NTD Modelling Consortium OPP1184344: CABP, GM; OPP1180644: SRP; OPP1191821: KO’R, MA). DFID/Wellcome Trust (Epidemic Preparedness Coronavirus research programme 221303/Z/20/Z: CABP, KvZ). Elrha R2HC/UK DFID/Wellcome Trust/This research was partly funded by the National Institute for Health Research (NIHR) using UK aid from the UK Government to support global health research. The views expressed in this publication are those of the author(s) and not necessarily those of the NIHR or the UK Department of Health and Social Care (KvZ). ERC Starting Grant (#757688: CJVA, KEA; #757699: JCE, MQ, RMGJH). This project has received funding from the European Union’s Horizon 2020 research and innovation programme—project EpiPose (101003688: KP, MJ, PK, WJE, YL). This research was partly funded by the Global Challenges Research Fund (GCRF) project ‘RECAP’ managed through RCUK and ESRC (ES/P010873/1: AG, CIJ). HDR UK (MR/S003975/1: RME). Nakajima Foundation (AE). NIHR (16/137/109: BJQ, CD, FYS, MJ, YL; Health Protection Research Unit for Modelling Methodology HPRU-2012-10096: NGD; PR-OD-1017-20002: AR). Royal Society (Dorothy Hodgkin Fellowship: RL; RP\EA\180004: PK). UK DHSC/UK Aid/NIHR (ITCRZ 03010: HPG). UK MRC (LID DTP MR/N013638/1: EMR; MC_PC 19065: RME; MR/P014658/1: GMK). Wellcome Trust (206250/Z/17/Z: AJK, TWR; 208812/Z/17/Z: SC, SFlasche; 210758/Z/18/Z: JDM, JH, NIB, SFunk, SRM). No funding (AKD, AMF, DCT, SH) Peer Reviewed CMMID Covid-19 Working Group: Rachel Lowe, Graham F. Medley & Oliver J. Brady

Emerging evidence suggests that contact tracing has had limited success in the UK in reducing the R number across the COVID-19 pandemic. We investigate potential pitfalls and areas for improvement by extending an existing branching process contact tracing model, adding diagnostic testing and refining parameter estimates. Our results demonstrate that reporting and adherence are the most important predictors of programme impact but tracing coverage and speed plus diagnostic sensitivity also play an important role. We conclude that well-implemented contact tracing could bring small but potentially important benefits to controlling and preventing outbreaks, providing up to a 15% reduction in R. We reaffirm that contact tracing is not currently appropriate as the sole control measure.

As several countries gradually release social distancing measures, rapid detection of new localized COVID-19 hotspots and subsequent intervention will be key to avoiding large-scale resurgence of transmission. We introduce ASMODEE (automatic selection of models and outlier detection for epidemics), a new tool for detecting sudden changes in COVID-19 incidence. Our approach relies on automatically selecting the best (fitting or predicting) model from a range of user-defined time series models, excluding the most recent data points, to characterize the main trend in an incidence. We then derive prediction intervals and classify data points outside this interval as outliers, which provides an objective criterion for identifying departures from previous trends. We also provide a method for selecting the optimal breakpoints, used to define how many recent data points are to be excluded from the trend fitting procedure. The analysis of simulated COVID-19 outbreaks suggests ASMODEE compares favourably with a state-of-art outbreak-detection algorithm while being simpler and more flexible. As such, our method could be of wider use for infectious disease surveillance. We illustrate ASMODEE using publicly available data of National Health Service (NHS) Pathways reporting potential COVID-19 cases in England at a fine spatial scale, showing that the method would have enabled the early detection of the flare-ups in Leicester and Blackburn with Darwen, two to three weeks before their respective lockdown. ASMODEE is implemented in the free R package trendbreaker. This article is part of the theme issue 'Modelling that shaped the early COVID-19 pandemic response in the UK'.

We explore strategies of contact tracing, case isolation and quarantine of exposed contacts to control the SARS-CoV-2 epidemic using a branching process model with household structure. This structure reflects higher transmission risks among household members than among non-household members. We explore strategic implementation choices that make use of household structure, and investigate strategies including two-step tracing, backwards tracing, smartphone tracing and tracing upon symptom report rather than test results. The primary model outcome is the effect of contact tracing, in combination with different levels of physical distancing, on the growth rate of the epidemic. Furthermore, we investigate epidemic extinction times to indicate the time period over which interventions must be sustained. We consider effects of non-uptake of isolation/quarantine, non-adherence, and declining recall of contacts over time. Our results find that, compared to self-isolation of cases without contact tracing, a contact tracing strategy designed to take advantage of household structure allows for some relaxation of physical distancing measures but cannot completely control the epidemic absent of other measures. Even assuming no imported cases and sustainment of moderate physical distancing, testing and tracing efforts, the time to bring the epidemic to extinction could be in the order of months to years. This article is part of the theme issue ‘Modelling that shaped the early COVID-19 pandemic response in the UK’.

The dynamics of immunity are crucial to understanding the long-term patterns of the SARS-CoV-2 pandemic. Several cases of reinfection with SARS-CoV-2 have been documented 48–142 days after the initial infection and immunity to seasonal circulating coronaviruses is estimated to be shorter than 1 year. Using an age-structured, deterministic model, we explore potential immunity dynamics using contact data from the UK population. In the scenario where immunity to SARS-CoV-2 lasts an average of three months for non-hospitalized individuals, a year for hospitalized individuals, and the effective reproduction number after lockdown ends is 1.2 (our worst-case scenario), we find that the secondary peak occurs in winter 2020 with a daily maximum of 387 000 infectious individuals and 125 000 daily new cases; threefold greater than in a scenario with permanent immunity. Our models suggest that longitudinal serological surveys to determine if immunity in the population is waning will be most informative when sampling takes place from the end of the lockdown in June until autumn 2020. After this period, the proportion of the population with antibodies to SARS-CoV-2 is expected to increase due to the secondary wave. Overall, our analysis presents considerations for policy makers on the longer-term dynamics of SARS-CoV-2 in the UK and suggests that strategies designed to achieve herd immunity may lead to repeated waves of infection as immunity to reinfection is not permanent.This article is part of the theme issue ‘Modelling that shaped the early COVID-19 pandemic response in the UK’.

Retrospective analyses into the non-pharmaceutical interventions (NPIs) used to combat the ongoing COVID-19 outbreak have highlighted the potential of optimizing interventions. These optimal interventions allow for policymakers to manage NPIs to minimize the epidemiological and human health impacts of both COVID-19 and the intervention itself. Here, we use a susceptible–infectious–recovered (SIR) mathematical model to explore the feasibility of optimizing the duration, magnitude and trigger point of five different NPI scenarios to minimize the peak prevalence or the attack rate of a simulated UK COVID-19 outbreak. An optimal parameter space to minimize the peak prevalence or the attack rate was identified for each intervention scenario, with each scenario differing with regard to how reductions to transmission were modelled. However, we show that these optimal interventions are fragile, sensitive to epidemiological uncertainty and prone to implementation error. We highlight the use of robust, but suboptimal interventions as an alternative, with these interventions capable of mitigating the peak prevalence or the attack rate over a broader, more achievable parameter space, but being less efficacious than theoretically optimal interventions. This work provides an illustrative example of the concept of intervention optimization across a range of different NPI strategies.This article is part of the theme issue ‘Modelling that shaped the early COVID-19 pandemic response in the UK’.

BackgroundRespiratory syncytial virus (RSV) is responsible for a significant burden of acute respiratory illness in children under 5 years old. Prior to rolling out any vaccination program, identification of the source of infant infections could further guide vaccination strategies.MethodsWe extended a dynamic model calibrated at the individual host level initially fit to social-temporal data on shedding patterns to include whole genome sequencing data available at a lower sampling intensity.ResultsIn this study population of 493 individuals with 55 infants under the age of 1 year distributed across 47 households, we found that 52% of RSV-B and 60% of RSV-A cases arose from infection within the household. Forty-five percent of infant infections appeared to occur in the household, of which 68% were a result of transmission from a child aged between 2 and 13 years living in the same household as the infant.ConclusionThese results further highlight the importance of pre-school and school-aged children in RSV transmission, particularly the role they play in directly infecting the household infant. These age groups are a potential RSV vaccination target group.