一类带有耐药性和细胞传播的HIV模型稳定性分析

研究了一类带有耐药性及细胞传播的HIV模型,得到了基本再生数R_s和R_r,建立了无病平衡点、两个边界平衡点以及地方病平衡点的全局渐近稳定的判定条件,通过Matlab数值模拟验证了结果的正确性.     

实施干预措施在HIV/AIDS预防中的效果

考虑了一类对高危人群实施干预措施的HIV/AIDS传播模型,给出了无病平衡点的全局稳定和地方病平衡点的局部稳定的条件.当R01时,讨论了地方病平衡点的局部渐进稳定性,重点讨论了对高危人群实施干预措施在HIV/AIDS预防中的积极效果.     

一类具有年龄结构和接种干预的手足口病模型动力学分析

考虑一类具有年龄结构且接种防疫措施的手足口病传染病模型，利用特征根法得到当基本再生数小于1时无病平衡点局部稳定，当基本再生数大于1时地方病平衡点局部稳定，通过构造Lyapunov函数研究了无病平衡点与地方病平衡点的全局稳定性.     

具有标准发生率和因病死亡率的离散SIRS传染病模型的全局稳定性

研究了一类具有标准发生率和因病死亡率的离散SIRS传染病模型,通过构造离散Lyapunov函数,得到了无病平衡点和地方病平衡点的全局渐近稳定性.特别地,当因病死亡率等于0时,地方病平衡点是全局渐近稳定的当且仅当基本再生数大于1.     

带有两个时滞的病毒动力学模型的稳定性

本文研究了带有饱和发生率和两个离散时滞的病毒动力学模型.通过构造Lyapunov函数和运用Lasalle不变原理,得到了模型的无病平衡点和地方病平衡点的全局渐近稳定性.当基本再生数R01时,模型的无病平衡点是全局渐进稳定的;当R01时,模型的地方病平衡点是全局渐进稳定的.     

具有体液免疫反应的时滞HIV模型的全局稳定性分析

研究了具有体液免疫反应的时滞HIV模型的全局稳定性,描述了HIV和T淋巴细胞、巨噬细胞的相互作用,得到模型的全局渐近稳定性是由基本再生数R0和免疫基本再生数R*0决定的.通过建立适当的Lyapunov函数,同时运用LaSalle不变原理得到,当R0≤1,R*0≤1R0和R0R*01时,对应的无病平衡点E0,无免疫平衡点E1和地方病平衡点E2是全局渐近稳定的.     

一类含潜伏时滞的SIS传染病模型的定性研究

利用构造Liapunov泛函的方法,研究了一类含有潜伏期时滞的SIS传染病模型.得到了地方病平衡点和无病平衡点局部及全局渐近稳定的充分条件;当时滞超过某一临界值时,地方病平衡点失去稳定性,通过Hopf分支在其附近跳出极限环.揭示了时滞对疾病传播的影响.     

对高危人群实施干预措施的时滞HIV/AIDS传播模型

考虑了一类对高危人群实施干预措施的HIV/AIDS传播模型,给出了无病平衡点的全局稳定和地方病平衡点局部稳定的条件,当R01时,疾病在人群中持久,同时,研究了干预措施在HIV/AIDS预防中的效果.     

丙型肝炎病毒感染流行病学模型的全局动态

主要研究了具有标准发生率的丙型肝炎流行病动力学模型.通过构造适当的Lyapunov函数,得到模型无病平衡点的全局稳定性以及特定条件下地方病平衡点的全局稳定性,即如果R₀≤1,模型的无病平衡点是全局渐近稳定的;如果R₀>1且μ=0,则地方病平衡点是全局渐近稳定的.     

具有非线性发生率的离散SIQ模型的稳定性分析

研究了具有非线性发生率的离散SIQ模型的稳定性.通过非标准差分方法得到了离散的SIQ模型,利用迭代法得到了模型解的正性和有界性、基于定义的基本再生数、无病平衡点和地方病平衡点的唯一存在性;通过线性化方法和构造离散Lyapunov函数方法得到了无病平衡点的稳定性;利用数值例子说明了地方病平衡点的稳定性结果.     

隐蔽期脉冲输注免疫因子HIV治疗模型的稳定性研究

考虑一类健康CD4＋T细胞、隐蔽期感染细胞和有效感染细胞的HIV治疗模型,得到了无脉冲免疫因子输注时治疗模型未感染平衡点和感染平衡点局部渐近稳定的充分条件;利用脉冲微分方程的比较定理和Floquent乘子理论获得了脉冲输注免疫因子时系统无病周期解的全局渐近稳定性充分条件以及健康细胞存活率范围;通过数值模拟验证了所获得的理论结论。     

一类具有Beddington-DeAngelis功能性反应的时滞HIV模型全局性分析

研究了一类四维的HIV传染病动力学时滞模型,模型使用的是Beddington-DeAngelis功能性反应形式的非线性发生率.考虑了受感染细胞CD4-T细胞的潜伏特性,也就是说被感染后没有传染性,只有被激活后才产生病毒细胞.通过构建Lyapunov函数,利用LaSalle不变集原理,给出了疾病平衡点,包括无病平衡点和地方性平衡点的全局渐近稳定.证明了当基本再生数小于1,无病平衡点全局渐近稳定;当基本再生数大于1,地方性平衡点全局也是渐近稳定.还考虑了具有n阶潜伏阶段的模型,并给出了平衡点的全局渐近稳定.     

具有非线性发生率和时滞的HIV感染模型分析

研究了一类具有Beddington-DeAngelis发生率和免疫反应时滞的艾滋病传染模型.首先通过构造适当的Lyapunov泛函并利用LaSalle不变原理证明了无病平衡点以及染病无免疫平衡点的全局渐近稳定性;其次讨论了感染免疫平衡点局部渐近稳定的充分条件,CTL免疫反应时滞可以改变感染免疫平衡点的稳定性并产生Hopf分支现象;最后利用数值模拟验证了以上结论.     

HIV preferentially infects HIV-specific CD4+ T cells

HIV infection is associated with the progressive loss of CD4(+) T cells through their destruction or decreased production. A central, yet unresolved issue of HIV disease is the mechanism for this loss, and in particular whether HIV-specific CD4(+) T cells are preferentially affected. Here we show that HIV-specific memory CD4(+) T cells in infected individuals contain more HIV viral DNA than other memory CD4(+) T cells, at all stages of HIV disease. Additionally, following viral rebound during interruption of antiretroviral therapy, the frequency of HIV viral DNA in the HIV-specific pool of memory CD4(+) T cells increases to a greater extent than in memory CD4(+) T cells of other specificities. These findings show that HIV-specific CD4(+) T cells are preferentially infected by HIV in vivo. This provides a potential mechanism to explain the loss of HIV-specific CD4(+) T-cell responses, and consequently the loss of immunological control of HIV replication. Furthermore, the phenomenon of HIV specifically infecting the very cells that respond to it adds a cautionary note to the practice of structured therapy interruption.     

Massive infection and loss of memory CD4+ T cells in multiple tissues during acute SIV infection

It has recently been established that both acute human immunodeficiency virus (HIV) and simian immunodeficiency virus (SIV) infections are accompanied by a dramatic and selective loss of memory CD4+ T cells predominantly from the mucosal surfaces. The mechanism underlying this depletion of memory CD4+ T cells (that is, T-helper cells specific to previously encountered pathogens) has not been defined. Using highly sensitive, quantitative polymerase chain reaction together with precise sorting of different subsets of CD4+ T cells in various tissues, we show that this loss is explained by a massive infection of memory CD4+ T cells by the virus. Specifically, 30-60% of CD4+ memory T cells throughout the body are infected by SIV at the peak of infection, and most of these infected cells disappear within four days. Furthermore, our data demonstrate that the depletion of memory CD4+ T cells occurs to a similar extent in all tissues. As a consequence, over one-half of all memory CD4+ T cells in SIV-infected macaques are destroyed directly by viral infection during the acute phase-an insult that certainly heralds subsequent immunodeficiency. Our findings point to the importance of reducing the cell-associated viral load during acute infection through therapeutic or vaccination strategies.     

HIV-specific cytotoxic T lymphocytes in seropositive individuals

Virus-specific cytotoxic T lymphocytes (CTL) which kill virus-infected cells are thought to be a major host defence against viral infections. Here we report the existence of human immunodeficiency virus (HIV)-specific CTL in persons infected with this virus, the aetiological agent of AIDS (acquired immunodeficiency syndrome). Recombinant HIV-vaccinia viruses were used to express HIV antigens in B-cell lines established from subjects seropositive for HIV and seronegative controls. Circulating lymphocytes capable of killing HIV env-expressing autologous B cells were detected in eight of eight seropositive subjects; in addition, at least three seropositive subjects demonstrated gag-specific cytotoxic responses. No HIV-specific cytotoxicity was observed in seronegative subjects. Selective inhibition of the env-specific cytotoxicity by a CD3-specific monoclonal antibody indicates that the effectors are T cells. This demonstration of a cytotoxic T-cell immune response to HIV in infected individuals should prove useful in investigating the immunopathogenesis of HIV infection further and in evaluating AIDS vaccine strategies.     

Cellular immune responses to HIV

The cellular immune response to the human immunodeficiency virus, mediated by T lymphocytes, seems strong but fails to control the infection completely. In most virus infections, T cells either eliminate the virus or suppress it indefinitely as a harmless, persisting infection. But the human immunodeficiency virus undermines this control by infecting key immune cells, thereby impairing the response of both the infected CD4+ T cells and the uninfected CD8+ T cells. The failure of the latter to function efficiently facilitates the escape of virus from immune control and the collapse of the whole immune system.     

乙肝病毒感染数量的一个数学模型

乙型肝炎是由乙型肝炎病毒(HBV)引起的肝病,该病毒干扰肝功能并造成病理损害.一小部分受感染者无法消灭该病毒而成为慢性感染,进而面临极高的死于肝硬化和肝癌的危险.乙型肝炎病毒通过与受感染者的血液或体液接触传播,这与人类免疫缺陷病毒(艾滋病毒)的方式相同.但是,乙型肝炎病毒的感染性比艾滋病毒高50至100倍.接种乙型肝炎疫苗是预防乙型肝炎的主要方法.如何有效防控乙肝的传染,不只是政府的事,也是每个国民应关注的问题.文章建立一个乙肝病毒传染的数学模型,并对模型进行实证分析;同时,对乙肝病毒的传染也做了一个预测.