Estimation and worldwide monitoring of the effective reproductive number of SARS-CoV-2
- ETH Zurich, Switzerland
- University of Basel, Switzerland
Abstract
The effective reproductive number Re is a key indicator of the growth of an epidemic. Since the start of the SARS-CoV-2 pandemic, many methods and online dashboards have sprung up to monitor this number through time. However, these methods are not always thoroughly tested, correctly placed in time, or are overly confident during high incidence periods. Here, we present a method for timely estimation of Re, applied to COVID-19 epidemic data from 170 countries. We thoroughly evaluate the method on simulated data, and present an intuitive web interface for interactive data exploration. We show that, in early 2020, in the majority of countries the estimated Re dropped below 1 only after the introduction of major non-pharmaceutical interventions. For Europe the implementation of non-pharmaceutical interventions was broadly associated with reductions in the estimated Re. Globally though, relaxing non-pharmaceutical interventions had more varied effects on subsequent Re estimates. Our framework is useful to inform governments and the general public on the status of epidemics in their country, and is used as the official source of Re estimates for SARS-CoV-2 in Switzerland. It further allows detailed comparison between countries and in relation to covariates such as implemented public health policies, mobility, behaviour, or weather data.
Data availability
- The source code of the pipeline is available at https://github.com/covid-19-Re/shiny-dailyRe ; this includes a script to download the required incidence data from public sources.- The resulting estimates (updated daily) are available at: https://github.com/covid-19-Re/dailyRe-Data- The code and data necessary to reproduce the figures in the paper is at: https://github.com/covid-19-Re/paper-codeThe Swiss estimates on our dashboard, and shown in Figs. 2, S9-S11 of the paper, use linelist data provided to us by the Federal Office of Public Health (FOPH) to inform the time-varying delay distributions. This data contains one row per infected individual, with information on their age, date of infection, postal code, etc. Although the data is anonymized, it could be linked directly to particular individuals, and this is a privacy concern. As such, we are not allowed to share the original data publicly. We are discussing with the FOPH whether we can share an aggregated form of the original data (for instance the time-varying delay distribution itself), but have already included the processed data (i.e. the estimates plotted in the figure) on https://github.com/covid-19-Re/paper-code for now.To obtain access to the original data, interested individuals should contact the FOPH directly. To the best of our knowledge, no official application or access granting procedure is in place, and applications will likely be assessed on a case by case basis.
Article and author information
Author details
Jana Sanne Huisman
Sebastian Bonhoeffer
Funding
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (31CA30_196267)
- Tanja Stadler
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (200021_172603)
- Marloes H Maathuis
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (310030B_176401)
- Sebastian Bonhoeffer
Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (407240-167121)
- Sebastian Bonhoeffer
- Tanja Stadler
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Miles P Davenport, University of New South Wales, Australia
Version history
- Preprint posted: November 30, 2020 (view preprint)
- Received: June 17, 2021
- Accepted: July 1, 2022
- Accepted Manuscript published: August 8, 2022 (version 1)
- Version of Record published: September 12, 2022 (version 2)
Copyright
© 2022, Huisman et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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Estimation and worldwide monitoring of the effective reproductive number of SARS-CoV-2
eLife 11:e71345.
https://doi.org/10.7554/eLife.71345
Further reading
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- Epidemiology and Global Health
Paxlovid, a SARS-CoV-2 antiviral, not only prevents severe illness but also curtails viral shedding, lowering transmission risks from treated patients. By fitting a mathematical model of within-host Omicron viral dynamics to electronic health records data from 208 hospitalized patients in Hong Kong, we estimate that Paxlovid can inhibit over 90% of viral replication. However, its effectiveness critically depends on the timing of treatment. If treatment is initiated three days after symptoms first appear, we estimate a 17% chance of a post-treatment viral rebound and a 12% (95% CI: 0%-16%) reduction in overall infectiousness for non-rebound cases. Earlier treatment significantly elevates the risk of rebound without further reducing infectiousness, whereas starting beyond five days reduces its efficacy in curbing peak viral shedding. Among the 104 patients who received Paxlovid, 62% began treatment within an optimal three-to-five-day day window after symptoms appeared. Our findings indicate that broader global access to Paxlovid, coupled with appropriately timed treatment, can mitigate the severity and transmission of SARS-Cov-2.
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- Epidemiology and Global Health
Background:
Circulating omega-3 and omega-6 polyunsaturated fatty acids (PUFAs) have been associated with various chronic diseases and mortality, but results are conflicting. Few studies examined the role of omega-6/omega-3 ratio in mortality.
Methods:
We investigated plasma omega-3 and omega-6 PUFAs and their ratio in relation to all-cause and cause-specific mortality in a large prospective cohort, the UK Biobank. Of 85,425 participants who had complete information on circulating PUFAs, 6461 died during follow-up, including 2794 from cancer and 1668 from cardiovascular disease (CVD). Associations were estimated by multivariable Cox proportional hazards regression with adjustment for relevant risk factors.
Results:
Risk for all three mortality outcomes increased as the ratio of omega-6/omega-3 PUFAs increased (all Ptrend <0.05). Comparing the highest to the lowest quintiles, individuals had 26% (95% CI, 15–38%) higher total mortality, 14% (95% CI, 0–31%) higher cancer mortality, and 31% (95% CI, 10–55%) higher CVD mortality. Moreover, omega-3 and omega-6 PUFAs in plasma were all inversely associated with all-cause, cancer, and CVD mortality, with omega-3 showing stronger effects.
Conclusions:
Using a population-based cohort in UK Biobank, our study revealed a strong association between the ratio of circulating omega-6/omega-3 PUFAs and the risk of all-cause, cancer, and CVD mortality.
Funding:
Research reported in this publication was supported by the National Institute of General Medical Sciences of the National Institute of Health under the award number R35GM143060 (KY). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
