In this work, we investigate an HIV-1 infection model with a general incidence rate and delayed CTL immune response. The model admits three possible equilibria, an infection-free equilibrium <span><em>E<...In this work, we investigate an HIV-1 infection model with a general incidence rate and delayed CTL immune response. The model admits three possible equilibria, an infection-free equilibrium <span><em>E</em></span><sup>*</sup><sub style="margin-left:-6px;">0</sub>, CTL-inactivated infection equilibrium <span><em>E</em></span><sup>*</sup><sub style="margin-left:-6px;">1</sub> and CTL-activated infection equilibrium <span><em>E</em></span><sup>*</sup><sub style="margin-left:-6px;">2</sub>. We prove that in the absence of CTL immune delay, the model has exactly the basic behaviour model, for all positive intracellular delays, the global dynamics are determined by two threshold parameters <em>R</em><sub>0</sub> and <em>R</em><sub>1</sub>, if <em>R</em><sub>0</sub> <span style="font-size:12px;white-space:nowrap;">≤</span> 1, <span><em>E</em></span><sup>*</sup><span style="margin-left:-6px;"><sub>0</sub> </span>is globally asymptotically stable, if <em>R</em><sub>1</sub> <span style="font-size:12px;white-space:nowrap;">≤</span> 1 < <em>R</em><sub>0</sub>, <span><em>E</em></span><sup>*</sup><span style="margin-left:-6px;"><sub>1</sub> </span>is globally asymptotically stable and if <em>R</em><sub>1</sub> >1, <span><em>E</em></span><sup>*</sup><span style="margin-left:-6px;"><sub>2</sub> </span>is globally asymptotically stable. But if the CTL immune response delay is different from zero, then the behaviour of the model at <span><em>E</em></span><sup>*</sup><span style="margin-left:-6px;"><sub>2</sub> </span>changes completely, although <em>R</em><sub>1</sub> > 1, a Hopf bifurcation at <span><em>E</em></span><sup>*</sup><span style="margin-left:-6px;"><sub>2</sub> </span>is established. In the end, we present some numerical simulations.展开更多
文摘In this work, we investigate an HIV-1 infection model with a general incidence rate and delayed CTL immune response. The model admits three possible equilibria, an infection-free equilibrium <span><em>E</em></span><sup>*</sup><sub style="margin-left:-6px;">0</sub>, CTL-inactivated infection equilibrium <span><em>E</em></span><sup>*</sup><sub style="margin-left:-6px;">1</sub> and CTL-activated infection equilibrium <span><em>E</em></span><sup>*</sup><sub style="margin-left:-6px;">2</sub>. We prove that in the absence of CTL immune delay, the model has exactly the basic behaviour model, for all positive intracellular delays, the global dynamics are determined by two threshold parameters <em>R</em><sub>0</sub> and <em>R</em><sub>1</sub>, if <em>R</em><sub>0</sub> <span style="font-size:12px;white-space:nowrap;">≤</span> 1, <span><em>E</em></span><sup>*</sup><span style="margin-left:-6px;"><sub>0</sub> </span>is globally asymptotically stable, if <em>R</em><sub>1</sub> <span style="font-size:12px;white-space:nowrap;">≤</span> 1 < <em>R</em><sub>0</sub>, <span><em>E</em></span><sup>*</sup><span style="margin-left:-6px;"><sub>1</sub> </span>is globally asymptotically stable and if <em>R</em><sub>1</sub> >1, <span><em>E</em></span><sup>*</sup><span style="margin-left:-6px;"><sub>2</sub> </span>is globally asymptotically stable. But if the CTL immune response delay is different from zero, then the behaviour of the model at <span><em>E</em></span><sup>*</sup><span style="margin-left:-6px;"><sub>2</sub> </span>changes completely, although <em>R</em><sub>1</sub> > 1, a Hopf bifurcation at <span><em>E</em></span><sup>*</sup><span style="margin-left:-6px;"><sub>2</sub> </span>is established. In the end, we present some numerical simulations.