Razvan G. Romanescu , Songdi Hu , Douglas Nanton , Mahmoud Torabi , Olivier Tremblay-Savard , Md Ashiqul Haque
{"title":"有效繁殖数量:建模和预测,并应用于多波新冠肺炎大流行。","authors":"Razvan G. Romanescu , Songdi Hu , Douglas Nanton , Mahmoud Torabi , Olivier Tremblay-Savard , Md Ashiqul Haque","doi":"10.1016/j.epidem.2023.100708","DOIUrl":null,"url":null,"abstract":"<div><p>Classical compartmental models of infectious disease assume that spread occurs through a homogeneous population. This produces poor fits to real data, because individuals vary in their number of epidemiologically-relevant contacts, and hence in their ability to transmit disease. In particular, network theory suggests that super-spreading events tend to happen more often at the beginning of an epidemic, which is inconsistent with the homogeneity assumption. In this paper we argue that a flexible decay shape for the effective reproductive number (<span><math><msub><mrow><mi>R</mi></mrow><mrow><mi>t</mi></mrow></msub></math></span>) indexed by the susceptible fraction (<span><math><msub><mrow><mi>S</mi></mrow><mrow><mi>t</mi></mrow></msub></math></span>) is a theory-informed modeling choice, which better captures the progression of disease incidence over human populations. This, in turn, produces better retrospective fits, as well as more accurate prospective predictions of observed epidemic curves. We extend this framework to fit multi-wave epidemics, and to accommodate public health restrictions on mobility. We demonstrate the performance of this model by doing a prediction study over two years of the SARS-CoV2 pandemic.</p></div>","PeriodicalId":49206,"journal":{"name":"Epidemics","volume":"44 ","pages":"Article 100708"},"PeriodicalIF":3.0000,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The effective reproductive number: Modeling and prediction with application to the multi-wave Covid-19 pandemic\",\"authors\":\"Razvan G. Romanescu , Songdi Hu , Douglas Nanton , Mahmoud Torabi , Olivier Tremblay-Savard , Md Ashiqul Haque\",\"doi\":\"10.1016/j.epidem.2023.100708\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><p>Classical compartmental models of infectious disease assume that spread occurs through a homogeneous population. This produces poor fits to real data, because individuals vary in their number of epidemiologically-relevant contacts, and hence in their ability to transmit disease. In particular, network theory suggests that super-spreading events tend to happen more often at the beginning of an epidemic, which is inconsistent with the homogeneity assumption. In this paper we argue that a flexible decay shape for the effective reproductive number (<span><math><msub><mrow><mi>R</mi></mrow><mrow><mi>t</mi></mrow></msub></math></span>) indexed by the susceptible fraction (<span><math><msub><mrow><mi>S</mi></mrow><mrow><mi>t</mi></mrow></msub></math></span>) is a theory-informed modeling choice, which better captures the progression of disease incidence over human populations. This, in turn, produces better retrospective fits, as well as more accurate prospective predictions of observed epidemic curves. We extend this framework to fit multi-wave epidemics, and to accommodate public health restrictions on mobility. We demonstrate the performance of this model by doing a prediction study over two years of the SARS-CoV2 pandemic.</p></div>\",\"PeriodicalId\":49206,\"journal\":{\"name\":\"Epidemics\",\"volume\":\"44 \",\"pages\":\"Article 100708\"},\"PeriodicalIF\":3.0000,\"publicationDate\":\"2023-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Epidemics\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1755436523000440\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"INFECTIOUS DISEASES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Epidemics","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1755436523000440","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"INFECTIOUS DISEASES","Score":null,"Total":0}
The effective reproductive number: Modeling and prediction with application to the multi-wave Covid-19 pandemic
Classical compartmental models of infectious disease assume that spread occurs through a homogeneous population. This produces poor fits to real data, because individuals vary in their number of epidemiologically-relevant contacts, and hence in their ability to transmit disease. In particular, network theory suggests that super-spreading events tend to happen more often at the beginning of an epidemic, which is inconsistent with the homogeneity assumption. In this paper we argue that a flexible decay shape for the effective reproductive number () indexed by the susceptible fraction () is a theory-informed modeling choice, which better captures the progression of disease incidence over human populations. This, in turn, produces better retrospective fits, as well as more accurate prospective predictions of observed epidemic curves. We extend this framework to fit multi-wave epidemics, and to accommodate public health restrictions on mobility. We demonstrate the performance of this model by doing a prediction study over two years of the SARS-CoV2 pandemic.
期刊介绍:
Epidemics publishes papers on infectious disease dynamics in the broadest sense. Its scope covers both within-host dynamics of infectious agents and dynamics at the population level, particularly the interaction between the two. Areas of emphasis include: spread, transmission, persistence, implications and population dynamics of infectious diseases; population and public health as well as policy aspects of control and prevention; dynamics at the individual level; interaction with the environment, ecology and evolution of infectious diseases, as well as population genetics of infectious agents.