Search

As the prevalence of viral infection in body, human T‐cell leukemia virus type 1 (HTLV‐1) is receiving increasing attention. Research on the corresponding virus models is of great significance to tackle the challenges of understanding HTLV‐1 development and treatment. This paper focuses on the dynamic analysis for a stochastic model with nonlinear cytotoxic T lymphocyte (CTL) response, which is driven by Ornstein–Uhlenbeck (OU) process to model the progression of HTLV‐1 in vivo. Rich dynamic behaviors such as the extinction of infected CD4+ T cells (ITCs), stationary distribution (SD), probability density, and finite‐time stability (FTS) of the model are established to reveal the interaction of cell populations. The optimal therapeutic strategy based on the cost‐benefit viewpoint is further obtained. Finally, illustrative numerical simulations are represented to corroborate the effectiveness of treatment and the ambient perturbation's impact that strengthening the noise strength can lead to rapid virus clearance. [ABSTRACT FROM AUTHOR]

This paper explores the dynamics analysis of a human immunodeficiency virus (HIV) model with saturated cytotoxic T lymphocyte (CTL) immune response and Beddington–DeAngelis infection rate. There are two time delays in the model to describe the time needed for infection of cell and CTL immune response generation, respectively. We obtain two thresholds and three possible equilibria from the model. By analyzing the corresponding characteristic equations, we study the stabilities of equilibrium and the effect of delays on CTL immune response. The results indicate that when immune delay is present, the steady state of equilibrium is disrupted and leads to a Hopf bifurcation. Finally, we use sensitivity analyses to show the effect of parameters on thresholds and numerical simulations to illustrate the theoretical results. [ABSTRACT FROM AUTHOR]

Malignant glioma is an aggressive primary brain tumor. Due to its location, the interactions of glioma and the immune system are complex. We start this paper by proposing a simple mathematical model that describes the interaction among glioma cells, microglia and cytotoxic T lymphocytes (CTLs). The existence and stability conditions of the equilibrium points are analyzed. Numerical results showed that neither microglia nor CTLs has the ability to eradicate the tumor. As a result, we extend the model by including the chemotherapeutic agent. The model has six equilibrium points, and one of these points represents a cured state. Through local stability, we found a range of values for the infusion rate that guarantees the elimination of glioma, as well as preventing the glioma from reoccurring. [ABSTRACT FROM AUTHOR]

In this paper, we develop a diffusive and delayed hepatitis B virus (HBV) infection model, which incorporates both virus‐to‐cell and cell‐to‐cell transmissions along with cytotoxic T lymphocyte (CTL) immune response. Two threshold parameters ℜ0$$ {\mathfrak{\Re}}_0 $$ (basic reproduction number) and ℜ1$$ {\mathfrak{\Re}}_1 $$ (immune response reproduction number) are defined, which determine the dynamic behavior of the model. Employing the approach of Lyapunov functionals, we show that the infection‐free steady state is globally asymptotically stable when ℜ0≤1$$ {\mathfrak{\Re}}_0\le 1 $$; the immune‐free infected steady state is globally asymptotically stable when ℜ1≤1<ℜ0$$ {\mathfrak{\Re}}_1\le 1<{\mathfrak{\Re}}_0 $$; and the immune‐present steady state is globally asymptotically stable when ℜ0>1,ℜ1>1$$ {\mathfrak{\Re}}_0>1,{\mathfrak{\Re}}_1>1 $$, and φ(I)=I$$ \varphi (I)=I $$. We perform the sensitivity and uncertainly analysis on ℜ0$$ {\mathfrak{\Re}}_0 $$ with respect to parameters and find that the most important parameter that drives the HBV infection is the mortality of HBV DNA capsids. Moreover, the theoretical results are supported with numerical simulations. [ABSTRACT FROM AUTHOR]

In this paper, using the methods of killing tumors and impulsive differential equations, two immunotherapy antitumor models for describing therapies of general tumors and advanced solid tumors are established. By using the theories of impulsive equations, small amplitude perturbation techniques, and the comparison technique, we obtain the conditions which guarantee the global asymptotical stability of the tumor‐eliminated periodic solution and system permanence, when immunotherapy alone is performed. The numerical results of the influences of the impulsive perturbation on the inherent oscillation show rich dynamics, such as period‐doubling bifurcation and chaos. Moreover, the effects of the combination of radiotherapy with immunotherapy on antitumor are obtained, including the threshold value of stability conditions of tumor‐eradication periodic solution when the mixed combination treatment of immunotherapy and radiotherapy is performed. Some numerical simulations for the effects of the timing of radiotherapy application and the timing of injection T cells on the threshold value are performed. Finally, we present some theoretical methods for suppressing the growth of tumors. [ABSTRACT FROM AUTHOR]

In this paper, we formulate a within‐host dynamics model for HIV/HTLV‐I co‐infection under the influence of cytotoxic T lymphocytes (CTLs). The model incorporates silent HIV‐infected CD4+T cells and silent HTLV‐infected CD4+T cells. The model includes two routes of HIV transmission, virus to cell (VTC) and cell to cell (CTC). It also incorporates two modes of HTLV‐I transmission, horizontal transmission via direct CTC contact and vertical transmission through mitotic division of Tax‐expressing HTLV‐infected cells. The model takes into account five types of distributed‐time delays. We analyze the model by proving the nonnegativity and boundedness of the solutions, calculating all possible equilibria, deriving a set of key threshold parameters, and proving the global stability of all equilibria. The global asymptotic stability of all equilibria is established by utilizing Lyapunov function and LaSalle's invariance principle. We present numerical simulations to justify the applicability and effectiveness of the theoretical results. In addition, we discuss the effect of HTLV‐I infection on the HIV dynamics and vice versa. [ABSTRACT FROM AUTHOR]

In this paper, the dynamics of stochastic human T‐cell leukemia virus type I (HTLV‐I) infection model with cytotoxic T lymphocyte (CTL) immune response is investigated. First, we show that the stochastic model exists as a unique positive global solution originating from the positive initial value. Second, we demonstrate that the stochastic model is stochastically permanent and stochastically ultimately bounded for any positive initial value. Third, we establish sufficient conditions for the existence of ergodic stationary distribution of the stochastic model. Fourth, the threshold R0∗ between extinction and persistence of the virus is obtained. Finally, numerical simulations are carried out to illustrate the theoretical results. [ABSTRACT FROM AUTHOR]

A two‐dimensional tumor‐immune model with the time delay of the adaptive immune response is considered in this paper. The model is designed to account for the interaction between cytotoxic T lymphocytes (CTLs) and cancer cells on the surface of a solid tumor. The model considers the surface growth as a major growth pattern of solid tumors in order to describe the existence of necrotic kernels. The qualitative analysis shows that the immune‐free equilibrium is unstable, and the behavior of positive equilibrium is closely related to the ratio of the immune killing rate to tumor volume growth rate. The positive equilibrium is locally asymptotically stable when the ratio is smaller than a critical value. Otherwise, the occurrence of the delay‐driven Hopf bifurcation at the positive equilibrium is proved. Applying the center manifold reduction and normal form method, we obtain explicit formulas to determine the properties of the Hopf bifurcation. The global continuation of a local Hopf bifurcation is investigated based on the coincidence degree theory. The results reveal that the time of the adaptive immune system taken to response to tumors can lead to oscillation dynamics. We also carry out detailed numerical analysis for parameters and numerical simulations to illustrate our qualitative analysis. Numerically, we find that shorter immune response time can lead to longer patient survival time, and the period and amplitude of a stable periodic solution increase with the increasing immune response time. When CTLs recruitment rate and death rate vary, we show how the ratio of the immune killing rate to tumor volume growth rate and the first bifurcation value change numerically, which yields further insights to the tumor‐immune dynamics. [ABSTRACT FROM AUTHOR]

A mathematical model of the tumor–immune system interactions is presented. The model includes the primary cell populations involved in CD4+ T cells mediated regression of the tumor, that is, tumor cells, CD4+ T cells, anti‐tumor cytokines, CTLA‐4 molecules, and normal cells. Our study reveals that host cells together with cytokines are key features in driving tumor dynamics. The malignant tumor can be completely suppressed if the tumor growth rate is small and the host cells are more competitive. No treatments are needed in this scenario as tumor cells are driven to extinction by host cells. We examine various immunotherapies of either T cells, anti‐tumor cytokines, anti‐CTLA‐4, or a combination of these to study their effectiveness. For the tumor with a medium growth rate and a moderate competitive ability to host cells, numerical simulations show that the host cells impel the tumor cells to demise due to battle with the normal cells and the effective jointed treatment strategy. [ABSTRACT FROM AUTHOR]