Yulian Kuryliak , Michael T.M. Emmerich , Dmytro Dosyn
{"title":"利用高效Gillespie算法模拟复杂网络上的疫情峰值动态","authors":"Yulian Kuryliak , Michael T.M. Emmerich , Dmytro Dosyn","doi":"10.1016/j.meegid.2025.105768","DOIUrl":null,"url":null,"abstract":"<div><div>We present an integrated study of epidemic spreading on complex networks that (i) reveals how network structure and targeted interventions shape the peak count of infected nodes (PCIN) and its timing, (ii) supplies an open-source dashboard that lets researchers explore these effects with realistic model extensions, and (iii) delivers a high-performance simulation engine which improves the time complexity of existing sparse network implementations of Gillespie's algorithm by multiplicative factors. Continuous-time SI/SIS/SIR dynamics are analyzed with respect to two intervention knobs: edge-specific infection rate reduction and node-level recovery acceleration, yielding explicit bounds on peak height and delay across heterogeneous topologies. To test scenarios interactively, we extend the dashboard simulator to include non-exponential recovery times, temporal rewiring, weighted and multi-type contacts, simulation of antigenically equivalent mutant strains, and a novel visual aggregation of likely infection routes. Moreover, we redesign Gillespie's algorithm for sparse graphs at its core by succinctly and incrementally updating the (sums of the) transition rate and maintaining a sorted infected node list, achieving speed increases with a multiplicative factor compared to the state-of-the-art implementation of the adjacency list. Additional speed gains can be achieved by our new algorithm when infection is in its early stage and only a few nodes of a large network are infected; a complementary dense matrix variant covers non-sparse cases. Benchmarks on Barabási–Albert networks confirm up-to-order-of-magnitude gains over the standard adjacency-list implementation of Gillespie's algorithm.</div></div>","PeriodicalId":54986,"journal":{"name":"Infection Genetics and Evolution","volume":"132 ","pages":"Article 105768"},"PeriodicalIF":2.6000,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Simulating epidemic peak dynamics on complex networks using efficient Gillespie algorithms\",\"authors\":\"Yulian Kuryliak , Michael T.M. Emmerich , Dmytro Dosyn\",\"doi\":\"10.1016/j.meegid.2025.105768\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>We present an integrated study of epidemic spreading on complex networks that (i) reveals how network structure and targeted interventions shape the peak count of infected nodes (PCIN) and its timing, (ii) supplies an open-source dashboard that lets researchers explore these effects with realistic model extensions, and (iii) delivers a high-performance simulation engine which improves the time complexity of existing sparse network implementations of Gillespie's algorithm by multiplicative factors. Continuous-time SI/SIS/SIR dynamics are analyzed with respect to two intervention knobs: edge-specific infection rate reduction and node-level recovery acceleration, yielding explicit bounds on peak height and delay across heterogeneous topologies. To test scenarios interactively, we extend the dashboard simulator to include non-exponential recovery times, temporal rewiring, weighted and multi-type contacts, simulation of antigenically equivalent mutant strains, and a novel visual aggregation of likely infection routes. Moreover, we redesign Gillespie's algorithm for sparse graphs at its core by succinctly and incrementally updating the (sums of the) transition rate and maintaining a sorted infected node list, achieving speed increases with a multiplicative factor compared to the state-of-the-art implementation of the adjacency list. Additional speed gains can be achieved by our new algorithm when infection is in its early stage and only a few nodes of a large network are infected; a complementary dense matrix variant covers non-sparse cases. Benchmarks on Barabási–Albert networks confirm up-to-order-of-magnitude gains over the standard adjacency-list implementation of Gillespie's algorithm.</div></div>\",\"PeriodicalId\":54986,\"journal\":{\"name\":\"Infection Genetics and Evolution\",\"volume\":\"132 \",\"pages\":\"Article 105768\"},\"PeriodicalIF\":2.6000,\"publicationDate\":\"2025-05-27\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Infection Genetics and Evolution\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1567134825000577\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"INFECTIOUS DISEASES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infection Genetics and Evolution","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1567134825000577","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"INFECTIOUS DISEASES","Score":null,"Total":0}
Simulating epidemic peak dynamics on complex networks using efficient Gillespie algorithms
We present an integrated study of epidemic spreading on complex networks that (i) reveals how network structure and targeted interventions shape the peak count of infected nodes (PCIN) and its timing, (ii) supplies an open-source dashboard that lets researchers explore these effects with realistic model extensions, and (iii) delivers a high-performance simulation engine which improves the time complexity of existing sparse network implementations of Gillespie's algorithm by multiplicative factors. Continuous-time SI/SIS/SIR dynamics are analyzed with respect to two intervention knobs: edge-specific infection rate reduction and node-level recovery acceleration, yielding explicit bounds on peak height and delay across heterogeneous topologies. To test scenarios interactively, we extend the dashboard simulator to include non-exponential recovery times, temporal rewiring, weighted and multi-type contacts, simulation of antigenically equivalent mutant strains, and a novel visual aggregation of likely infection routes. Moreover, we redesign Gillespie's algorithm for sparse graphs at its core by succinctly and incrementally updating the (sums of the) transition rate and maintaining a sorted infected node list, achieving speed increases with a multiplicative factor compared to the state-of-the-art implementation of the adjacency list. Additional speed gains can be achieved by our new algorithm when infection is in its early stage and only a few nodes of a large network are infected; a complementary dense matrix variant covers non-sparse cases. Benchmarks on Barabási–Albert networks confirm up-to-order-of-magnitude gains over the standard adjacency-list implementation of Gillespie's algorithm.
期刊介绍:
(aka Journal of Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases -- MEEGID)
Infectious diseases constitute one of the main challenges to medical science in the coming century. The impressive development of molecular megatechnologies and of bioinformatics have greatly increased our knowledge of the evolution, transmission and pathogenicity of infectious diseases. Research has shown that host susceptibility to many infectious diseases has a genetic basis. Furthermore, much is now known on the molecular epidemiology, evolution and virulence of pathogenic agents, as well as their resistance to drugs, vaccines, and antibiotics. Equally, research on the genetics of disease vectors has greatly improved our understanding of their systematics, has increased our capacity to identify target populations for control or intervention, and has provided detailed information on the mechanisms of insecticide resistance.
However, the genetics and evolutionary biology of hosts, pathogens and vectors have tended to develop as three separate fields of research. This artificial compartmentalisation is of concern due to our growing appreciation of the strong co-evolutionary interactions among hosts, pathogens and vectors.
Infection, Genetics and Evolution and its companion congress [MEEGID](http://www.meegidconference.com/) (for Molecular Epidemiology and Evolutionary Genetics of Infectious Diseases) are the main forum acting for the cross-fertilization between evolutionary science and biomedical research on infectious diseases.
Infection, Genetics and Evolution is the only journal that welcomes articles dealing with the genetics and evolutionary biology of hosts, pathogens and vectors, and coevolution processes among them in relation to infection and disease manifestation. All infectious models enter the scope of the journal, including pathogens of humans, animals and plants, either parasites, fungi, bacteria, viruses or prions. The journal welcomes articles dealing with genetics, population genetics, genomics, postgenomics, gene expression, evolutionary biology, population dynamics, mathematical modeling and bioinformatics. We also provide many author benefits, such as free PDFs, a liberal copyright policy, special discounts on Elsevier publications and much more. Please click here for more information on our author services .