Viral infection dynamics with mitosis, intracellular delays and immune response.
Viral infection dynamics with mitosis, intracellular delays and immune response.
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DOI：
10.3934/mbe.2023139
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发表时间：
2023-01
期刊：
影响因子：
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通讯作者：
Jia-wen Deng;Ping Jiang;Hongying Shu
中科院分区：
文献类型：
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作者：
Jia-wen Deng;Ping Jiang;Hongying Shu
在本文中，我们提出了一个具有未感染的靶细胞有丝分裂的延迟病毒感染模型，有两种感染模式(病毒到细胞传播和细胞到细胞传播)和免疫反应。该模型涉及病毒感染、病毒生产和CTL招募过程中的细胞内延迟。我们证明了阈值动力学由感染的基本再生数$R_0和免疫反应的基本再生数$R_{IM}$决定。当$R_{IM}>；1$时，模型动力学变得非常丰富。在这种情况下，我们使用CTLS招募延迟$\tau_3作为分叉参数来获得模型系统正平衡点和全局Hopf分岔图上的稳定性开关。这使得我们可以证明，$tau_3$可以导致多个稳定性开关，多个稳定周期解的共存，甚至混沌。两参数分支分析的简单模拟表明，CTL招募延迟$tau_3和有丝分裂率$r都对病毒动力学有很大的影响，但它们的表现不同。
In this paper, we propose a delayed viral infection model with mitosis of uninfected target cells, two infection modes (virus-to-cell transmission and cell-to-cell transmission), and immune response. The model involves intracellular delays during the processes of viral infection, viral production, and CTLs recruitment. We verify that the threshold dynamics are determined by the basic reproduction number $ R_0 $ for infection and the basic reproduction number $ R_{IM} $ for immune response. The model dynamics become very rich when $ R_{IM} > 1 $. In this case, we use the CTLs recruitment delay $ \tau_3 $ as the bifurcation parameter to obtain stability switches on the positive equilibrium and global Hopf bifurcation diagrams for the model system. This allows us to show that $ \tau_3 $ can lead to multiple stability switches, the coexistence of multiple stable periodic solutions, and even chaos. A brief simulation of two-parameter bifurcation analysis indicates that both the CTLs recruitment delay $ \tau_3 $ and the mitosis rate $ r $ have a strong impact on the viral dynamics, but they do behave differently.