Global stability is analyzed for a general mathematical model of HIV-1 pathogenesis proposed by Nelson and Perelson [11]. The general model include two distributed intracellular delays and a combination therapy with a reverse transcriptase inhibitor and a protease inhibitor. It is shown that the model exhibits a threshold dynamics: if the basic reproduction number is less than or equal to one, then the HIV-1 infection is cleared from the T-cell population; whereas if the basic reproduction number is larger than one, then the HIV-1 infection persists and the viral concentration maintains at a constant level.

In this paper, we propose and analyze a delayed HIV-1 model with CTL immune response and virus waning. The two discrete delays stand for the time for infected cells to produce viruses after viral entry and for the time for CD$8^+$ T cell immune response to emerge to control viral replication. We obtain the positiveness and boundedness of solutions and find the basic reproduction number $R_0$. If $R_01$, then the system is uniformly persistent and the viral concentration maintains at some constant level. The global dynamics when $R_0>1$ is complicated. We establish the local stability of the infected steady state and show that Hopf bifurcation can occur. Both analytical and numerical results indicate that if, in the initial infection stage,the effect of delays on HIV-1 infection is ignored, then the risk of HIV-1 infection (if persists) will be underestimated. Moreover, the viral load differs from that without virus waning. These results highlight the important role of delays and virus waning on HIV-1 infection.<!--1--> <!--1-->