A modelling approach to estimate the transmissibility of SARS-CoV-2 during periods of high, low, and zero case incidence
- Curtin University, Australia
- University of Melbourne, Australia
- Telethon Kids Institute, Australia
Abstract
Against a backdrop ofwidespread global transmission, a number of countries have successfully brought large outbreaks of COVID-19 under control and maintained near-elimination status. A key element of epidemic response is the tracking of disease transmissibility in near real-time. During major out-breaks, the effective reproduction number can be estimated froma time-series of case, hospitalisation or death counts. In low or zero incidence settings, knowing the potential for the virus to spread is a response priority. Absence of case data means that this potential cannot be estimated directly. We present a semi-mechanisticmodelling framework that draws on time-series of both behavioural data and case data (when disease activity is present) to estimate the transmissibility of SARS-CoV-2 fromperiods of high to low- or zero- case incidence, with a coherent transition in interpretation across the changing epidemiological situations. Of note, during periods of epidemic activity, our analysis recovers the effective reproduction number, while during periods of low- or zero- case incidence, it provides an estimate of transmission risk. This enables tracking and planning of progress towards the control of large outbreaks, maintenance of virus suppression, and monitoring the risk posed by re-introduction of the virus. We demonstrate the value of our methods by reporting on their use throughout 2020 in Australia, where they have become a central component of the national COVID-19 response.
Data availability
Datasets analysed and generated during this study are available at the following link: https://figshare.com/s/0e13ccc2f731149d45d1. For estimates of the time-varying effective reproduction number and transmission potential (Figure 2), the complete line listed data within the Australian national COVID-19 database are not publicly available. However, we provide the cases per day by notification date and state (Data files 1 and 2) which, when supplemented with the estimated distribution of the delay from symptom onset to notification as in Figure 3D and H (provided in Data files 3 and 4), and Data files 5-10, analyses of the time-varying effective reproduction number and transmission potential can be performed. Data files 5-10 contain the numerical data, output from each of the model components, used to generate Figure 3. For access to the raw data, a request must be submitted via NNDSS.datarequests@health.gov.au which will be assessed by a data committee.Model code for performing the analyses and generating the figures is available at: https://github.com/goldingn/covid19_australia_interventions
Article and author information
Author details
Funding
Australian Government
- Nick Golding
- David J Price
- Gerard Ryan
- Jodie McVernon
- James M McCaw
- Freya M Shearer
Australian Research Council (DE180100635)
- Nick Golding
National Health and Medical Research Council (GNT1170960)
- Jodie McVernon
- James M McCaw
National Health and Medical Research Council (GNT1117140)
- Jodie McVernon
National Health and Medical Research Council (2021/GNT2010051)
- Freya M Shearer
World Health Organization
- Nick Golding
- David J Price
- Gerard Ryan
- Jodie McVernon
- James M McCaw
- Freya M Shearer
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Ethics
Human subjects: The study was undertaken as urgent public health action to support Australia's COVID-19 pandemic response. The study used data from the Australian National Notifiable Disease Surveillance System (NNDSS) provided to the Australian Government Department of Health under the National Health Security Agreement for the purposes of national communicable disease surveillance. Data from the NNDSS were supplied after de-identification to the investigator team for the purposes of provision of epidemiological advice to government. Contractual obligations established strict data protection protocols agreed between the University of Melbourne and sub-contractors and the Australian Government Department of Health, with oversight and approval for use in supporting Australia's pandemic response and for publication provided by the data custodians represented by the Communicable Diseases Network of Australia. The ethics of the use of these data for these purposes, including publication, was agreed by the Department of Health with the Communicable Diseases Network of Australia.
Copyright
© 2023, Golding 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.
Metrics
-
- 1,131
- views
-
- 180
- downloads
-
- 19
- citations
Views, downloads and citations are aggregated across all versions of this paper published by eLife.
Download links
A two-part list of links to download the article, or parts of the article, in various formats.
Downloads (link to download the article as PDF)
Open citations (links to open the citations from this article in various online reference manager services)
Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)
A modelling approach to estimate the transmissibility of SARS-CoV-2 during periods of high, low, and zero case incidence
eLife 12:e78089.
https://doi.org/10.7554/eLife.78089
Further reading
-
- Epidemiology and Global Health
- Genetics and Genomics
Alzheimer’s disease (AD) is a complex degenerative disease of the central nervous system, and elucidating its pathogenesis remains challenging. In this study, we used the inverse-variance weighted (IVW) model as the major analysis method to perform hypothesis-free Mendelian randomization (MR) analysis on the data from MRC IEU OpenGWAS (18,097 exposure traits and 16 AD outcome traits), and conducted sensitivity analysis with six models, to assess the robustness of the IVW results, to identify various classes of risk or protective factors for AD, early-onset AD, and late-onset AD. We generated 400,274 data entries in total, among which the major analysis method of the IVW model consists of 73,129 records with 4840 exposure traits, which fall into 10 categories: Disease, Medical laboratory science, Imaging, Anthropometric, Treatment, Molecular trait, Gut microbiota, Past history, Family history, and Lifestyle trait. More importantly, a freely accessed online platform called MRAD (https://gwasmrad.com/mrad/) has been developed using the Shiny package with MR analysis results. Additionally, novel potential AD therapeutic targets (CD33, TBCA, VPS29, GNAI3, PSME1) are identified, among which CD33 was positively associated with the main outcome traits of AD, as well as with both EOAD and LOAD. TBCA and VPS29 were negatively associated with the main outcome traits of AD, as well as with both EOAD and LOAD. GNAI3 and PSME1 were negatively associated with the main outcome traits of AD, as well as with LOAD, but had no significant causal association with EOAD. The findings of our research advance our understanding of the etiology of AD.
-
- Epidemiology and Global Health
Artificially sweetened beverages containing noncaloric monosaccharides were suggested as healthier alternatives to sugar-sweetened beverages. Nevertheless, the potential detrimental effects of these noncaloric monosaccharides on blood vessel function remain inadequately understood. We have established a zebrafish model that exhibits significant excessive angiogenesis induced by high glucose, resembling the hyperangiogenic characteristics observed in proliferative diabetic retinopathy (PDR). Utilizing this model, we observed that glucose and noncaloric monosaccharides could induce excessive formation of blood vessels, especially intersegmental vessels (ISVs). The excessively branched vessels were observed to be formed by ectopic activation of quiescent endothelial cells (ECs) into tip cells. Single-cell transcriptomic sequencing analysis of the ECs in the embryos exposed to high glucose revealed an augmented ratio of capillary ECs, proliferating ECs, and a series of upregulated proangiogenic genes. Further analysis and experiments validated that reduced foxo1a mediated the excessive angiogenesis induced by monosaccharides via upregulating the expression of marcksl1a. This study has provided new evidence showing the negative effects of noncaloric monosaccharides on the vascular system and the underlying mechanisms.
