Global stability of an HIV-1 model with distributed intracellular delays and a combination therapy.
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.
Liu
Shengqiang
S
Academy of Fundamental and Interdisciplinary Sciences, Harbin Institute of Technology, 3041#, 2 Yi-Kuang Street, Harbin, 150080, China. sqliu@hit.edu.cn
Wang
Lin
L
D019380:Anti-HIV Agents / Q000627:therapeutic use*; D004359:Drug Therapy, Combination; D015658:HIV Infections / Q000188:drug therapy* / Q000276:immunology / Q000821:virology*; D017320:HIV Protease Inhibitors / Q000627:therapeutic use; D015497:HIV-1 / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D018894:Reverse Transcriptase Inhibitors / Q000627:therapeutic use; D013601:T-Lymphocytes / Q000276:immunology
D019380:Anti-HIV Agents; D017320:HIV Protease Inhibitors; D018894:Reverse Transcriptase Inhibitors