Optimal control of a delayed hepatitis B viral infection model with HBV DNA-containing capsids and CTL immune response

2018 ◽  
Vol 39 (3) ◽  
pp. 1262-1272 ◽  
Author(s):  
Jaouad Danane ◽  
Adil Meskaf ◽  
Karam Allali
2017 ◽  
Vol 10 (02) ◽  
pp. 1750020 ◽  
Author(s):  
Jianhua Pang ◽  
Jing-An Cui

In this paper, a hepatitis B viral infection model with a density-dependent proliferation rate of cytotoxic T lymphocyte (CTL) cells and immune response delay is investigated. By analyzing the model, we show that the virus-free equilibrium is globally asymptotically stable, if the basic reproductive ratio is less than one and an endemic equilibrium exists if the basic reproductive ratio is greater than one. By using the stability switches criterion in the delay-differential system with delay-dependent parameters, we present that the stability of endemic equilibrium changes and eventually become stable as time delay increases. This means majority of hepatitis B infection would eventually become a chronic infection due to the immune response time delay is fairly long. Numerical simulations are carried out to explain the mathematical conclusions and biological implications.


Computation ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 21 ◽  
Author(s):  
Khalid Hattaf

In this paper, we propose and investigate a diffusive viral infection model with distributed delays and cytotoxic T lymphocyte (CTL) immune response. Also, both routes of infection that are virus-to-cell infection and cell-to-cell transmission are modeled by two general nonlinear incidence functions. The well-posedness of the proposed model is also proved by establishing the global existence, uniqueness, nonnegativity and boundedness of solutions. Moreover, the threshold parameters and the global asymptotic stability of equilibria are obtained. Furthermore, diffusive and delayed virus dynamics models presented in many previous studies are improved and generalized.


2019 ◽  
Vol 29 (12) ◽  
pp. 1950161 ◽  
Author(s):  
Jinhu Xu ◽  
Yan Geng ◽  
Suxia Zhang

We have developed a class of viral infection model with cell-to-cell transmission and humoral immune response. The model addresses both immune and intracellular delays. We also constructed Lyapunov functionals to establish the global dynamical properties of the equilibria. Theoretical results indicate that considering only two intracellular delays did not affect the dynamical behavior of the model, but incorporating an immune delay greatly affects the dynamics, i.e. an immune delay may destabilize the immunity-activated equilibrium and lead to Hopf bifurcation, oscillations and stability switches. Our results imply that an immune delay dominates the intracellular delays in the model. We also investigated the direction of the Hopf bifurcation and the stability of the periodic solutions by applying normal form and center manifold theory, and investigated the existence of global Hopf bifurcation by regarding the immune delay as a bifurcation parameter. Numerical simulations are carried out to support the analytical conclusions.


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