{"title":"具有 CTL 免疫反应、分布式延迟和饱和发病率的细胞因子增强病毒感染模型","authors":"Xiaodong Cao, Songbo Hou, Xiaoqing Kong","doi":"arxiv-2409.10223","DOIUrl":null,"url":null,"abstract":"In this paper, we propose a delayed cytokine-enhanced viral infection model\nincorporating saturation incidence and immune response. We compute the basic\nreproduction numbers and introduce a convex cone to discuss the impact of\nnon-negative initial data on solutions. By defining appropriate Lyapunov\nfunctionals and employing LaSalle's invariance principle, we investigate the\nstability of three equilibria: the disease-free equilibrium, the\nimmunity-inactivated equilibrium, and the immunity-activated equilibrium. We\nestablish conditions under which these equilibria are globally asymptotically\nstable. Numerical analyses not only corroborate the theoretical results but\nalso reveal that intervention in virus infection can be achieved by extending\nthe delay period.","PeriodicalId":501035,"journal":{"name":"arXiv - MATH - Dynamical Systems","volume":"1 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"A cytokine-enhanced viral infection model with CTL immune response, distributed delay and saturation incidence\",\"authors\":\"Xiaodong Cao, Songbo Hou, Xiaoqing Kong\",\"doi\":\"arxiv-2409.10223\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"In this paper, we propose a delayed cytokine-enhanced viral infection model\\nincorporating saturation incidence and immune response. We compute the basic\\nreproduction numbers and introduce a convex cone to discuss the impact of\\nnon-negative initial data on solutions. By defining appropriate Lyapunov\\nfunctionals and employing LaSalle's invariance principle, we investigate the\\nstability of three equilibria: the disease-free equilibrium, the\\nimmunity-inactivated equilibrium, and the immunity-activated equilibrium. We\\nestablish conditions under which these equilibria are globally asymptotically\\nstable. Numerical analyses not only corroborate the theoretical results but\\nalso reveal that intervention in virus infection can be achieved by extending\\nthe delay period.\",\"PeriodicalId\":501035,\"journal\":{\"name\":\"arXiv - MATH - Dynamical Systems\",\"volume\":\"1 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-09-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"arXiv - MATH - Dynamical Systems\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/arxiv-2409.10223\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"arXiv - MATH - Dynamical Systems","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/arxiv-2409.10223","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
A cytokine-enhanced viral infection model with CTL immune response, distributed delay and saturation incidence
In this paper, we propose a delayed cytokine-enhanced viral infection model
incorporating saturation incidence and immune response. We compute the basic
reproduction numbers and introduce a convex cone to discuss the impact of
non-negative initial data on solutions. By defining appropriate Lyapunov
functionals and employing LaSalle's invariance principle, we investigate the
stability of three equilibria: the disease-free equilibrium, the
immunity-inactivated equilibrium, and the immunity-activated equilibrium. We
establish conditions under which these equilibria are globally asymptotically
stable. Numerical analyses not only corroborate the theoretical results but
also reveal that intervention in virus infection can be achieved by extending
the delay period.