一类具有饱和发生率和分布时滞的HIV感染模型的全局稳定性分析

建立了一类具有饱和发生率和分布时滞的HIV感染模型,给出了病毒感染再生数R0和CTL免疫再生数R1,证明了:当R0≤1时,未感染平衡点是全局稳定的;当R0>1>R1时,无免疫感染平衡点是全局稳定的;当R1>1时,免疫感染平衡点是全局稳定的.     

一类具有饱和发生率和分布时滞的HIV感染模型的全局稳定性分析

建立了一类具有饱和发生率和分布时滞的HIV感染模型,给出了病毒感染再生数R0和CTL免疫再生数R1,证明了:当R0≤1时,未感染平衡点是全局稳定的;当R01R1时,无免疫感染平衡点是全局稳定的;当R11时,免疫感染平衡点是全局稳定的.     

考虑CTL免疫反应的病毒动力学模型的全局稳定性分析

利用Lyapunov函数方法研究了CTL免疫反应的病毒动力学模型的全局稳定性．当基本再生数R0≤1，病毒在体内清除；而R0〉1时，病毒在体内持续生存，并且模型的正解当CTL免疫再生数R1≤1时趋于无免疫平衡点，R1〉1时趋于正平衡点．     

一类有迁移的传染病模型的阈值

建立了一类种群有迁移的流行病模型，得到了这类模型的基本再生数R0，证明了如果R0〈1，则无病平衡点是全局渐近稳定的；如果R0〉1，则地方病平衡点存在，且是全局渐近稳定的，即R0是一个阈值．     

具有饱和发生率和分布时滞的HIV免疫模型的稳定性

本文提出一类具有饱和发生率和抗体免疫反应的细胞内感染的时滞HIV感染模型，包括未感染细胞、潜伏感染细胞、感染细胞、游离HIV病毒和CTL免疫反应细胞。考虑4种时滞：潜伏感染时滞、细胞内时滞、感染细胞转化病毒时滞和CTL免疫反应时滞。定义2个阈值：感染基本再生数R₀和CTL免疫再生数R₁,得到了模型的3类平衡点：无感染平衡点、免疫灭活感染平衡点和免疫激活感染平衡点。通过分析特征方程、构造Lyapunov函数和LaSalle不变原理，建立了各平衡点局部以及全局渐近稳定性的判定准则。     

考虑病毒DNA核衣壳和细胞-细胞感染的HBV感染模型的阈值动力学研究

为研究HBV DNA核衣壳和“细胞-细胞”感染对HBV感染过程的影响,建立了一类具有病毒DNA核衣壳和细胞-细胞感染的HBV感染模型,给出模型的基本再生数,并使用Routh-Hurwitz判据和Lyapunov稳定性理论得到基本再生数的阈值动力学性质.即如果基本再生数小于1,则无病毒感染平衡点是全局渐近稳定的;如果基本再生数大于1,则病毒感染平衡态是全局渐近稳定的.结合Matlab数值模拟验证了模型的理论结果,并揭示细胞-细胞感染将低估HBV感染过程中感染细胞和病毒载量的最终水平.     

具有两类靶细胞的病毒感染模型的全局稳定性

研究了具有两类靶细胞和CTL免疫应答与抗体免疫反应的时滞病毒感染模型的动力学行为.模型描述了病毒和两类细胞的相互作用:CD4+T淋巴细胞与巨噬细胞.通过构造适当的Lyapunov泛函,使用LaSalle不变性原理,证明了CD4+T淋巴细胞和巨噬细胞的基本再生总数R0、CTL免疫再生数R1、抗体免疫再生数R2、CTL免疫竞争再生数R3和抗体免疫竞争再生数R4决定了模型的全局性态.若R0≤1,病毒在体内清除.若R01,正解在R1≤1,R2≤1时趋于无免疫平衡点,在R11≥R4时趋于CTL主导平衡点,在R21≥R3时趋于抗体主导平衡点,在R31且R41时趋于正平衡点,获得了无病平衡点、无免疫平衡点、CTL主导平衡点、抗体主导平衡点和正平衡点全局渐近稳定的充分条件.     

一类捕食——被捕食种群系统的定性分析

本文讨论一类具有常数存放率与收获率的捕食—被捕食两种群系统．其数学模型为（1），当h＞0，x0＞D时，得到正平衡点R（x，y）为全局稳定的结论，当h＜0，＜BD＜1时，正平衡点R（x，y）周围不存在极限环，当h＜0，＜BD＜1，x＜D＜x2时，正平衡点R（x，y）为全局稳定．     

外源性透明质酸减少R5-HIV对CD4~+T细胞感染的研究（英文）

目的探讨外源性透明质酸(HA)是否可以降低巨噬细胞嗜性(CCR5依赖,R5)人类免疫缺陷病毒(HIV)对CD4+T细胞的感染性。方法首先用TZM-bl细胞和未受刺激的CD4+T细胞检测,以评估外源性透明质酸(HA)能否降低R5-HIV的感染性。用透明质酸酶去处理未受刺激的CD4+T细胞,研究内源性HA对R5-HIV感染性的影响。最后,同时测量外源性和内源性透明质酸(HA)对R5-HIV对CD4+T细胞粘和力的影响。结果 (1)100μg外源性HA处理能够显著降低R5-HIV感染TZM-bl细胞和未受刺激的CD4+T细胞(P<0.001)。(2)透明质酸酶处理可增强HIV的感染性,但是如果加上100μg外源性HA可以逆转透明质酸酶的处理(P<0.001)。(3)100μg外源性HA可以减少R5-HIV对CD4+T细胞的粘和力,透明质酸酶处理可以提高R5-HIV对CD4+T细胞的粘和力(P<0.001)。结论外源性HA减少R5-HIV对未受刺激的CD4+T细胞的感染性,而透明质酸酶处理可以提高R5-HIV对CD4+T细胞的粘和力,能增强R5-HIV对CD4+T细胞的感染性。     

具有B-D功能反映函数和T淋巴细胞免疫的病毒动力学模型稳定性

文章研究了B-D功能反映函数接触率和T淋巴细胞免疫的病毒模型稳定性.通过构造Lyapunov函数和利用LaSalle不变集原理,对模型的三个平衡点全局稳定性进行了分析,得到:(1)当R0≤1时,无病平衡点E0全局渐近稳定的;(2)当R01,R1≤1时,地方病平衡点E1是全局渐近稳定性;(3)当R11时,免疫病平衡点E2全局渐近稳定性.     

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.     

考虑免疫反应损害的细胞-细胞病毒动力学模型的确定和随机稳定性分析

利用Lyapunov函数方法研究了在免疫反应损害情况下的细胞细胞病毒动力学模型的确定稳定性和随机稳定性.当基本再生数R0≤1,病毒在体内清除;而R0>1时,病毒在体内持续生存.并且模型的正平衡点在随机扰动下也是稳定的.     

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.     

Transmission of the polyoma virus middle T gene as the oncogene of a murine retrovirus

Polyoma virus is a papovavirus that productively infects mouse cells. In cells of other species, such as rat cells, polyoma virus is virtually unable to replicate, and a small proportion of infected cells become stably transformed. The ability of polyoma virus to transform infected cells is determined by genes that encode the large, middle and small T antigens and which are found in the early region of the virus genome. We have inserted the transforming region of polyoma virus into a murine leukaemia virus (MLV) vector, to generate a replication-defective transforming retrovirus which for the first time allows efficient transformation of mouse cells by the polyoma virus middle T gene. During the life cycle of this recombinant virus the intervening sequence present in the original polyoma virus middle T gene was removed. The recombinant virus that we have constructed is analogous to other acutely transforming retroviruses, and demonstrates that the polyoma middle T gene is a dominant transforming oncogene.     

Peak SIV replication in resting memory CD4+ T cells depletes gut lamina propria CD4+ T cells

In early simian immunodeficiency virus (SIV) and human immunodeficiency virus-1 (HIV-1) infections, gut-associated lymphatic tissue (GALT), the largest component of the lymphoid organ system, is a principal site of both virus production and depletion of primarily lamina propria memory CD4+ T cells; that is, CD4-expressing T cells that previously encountered antigens and microbes and homed to the lamina propria of GALT. Here, we show that peak virus production in gut tissues of SIV-infected rhesus macaques coincides with peak numbers of infected memory CD4+ T cells. Surprisingly, most of the initially infected memory cells were not, as expected, activated but were instead immunophenotypically 'resting' cells that, unlike truly resting cells, but like the first cells mainly infected at other mucosal sites and peripheral lymph nodes, are capable of supporting virus production. In addition to inducing immune activation and thereby providing activated CD4+ T-cell targets to sustain infection, virus production also triggered an immunopathologically limiting Fas-Fas-ligand-mediated apoptotic pathway in lamina propria CD4+ T cells, resulting in their preferential ablation. Thus, SIV exploits a large, resident population of resting memory CD4+ T cells in GALT to produce peak levels of virus that directly (through lytic infection) and indirectly (through apoptosis of infected and uninfected cells) deplete CD4+ T cells in the effector arm of GALT. The scale of this CD4+ T-cell depletion has adverse effects on the immune system of the host, underscoring the importance of developing countermeasures to SIV that are effective before infection of GALT.     

一类具有饱和感染率的病毒动力学模型的全局稳定性

研究了一类HIV感染的病毒动力学模型,得到了病毒消除与否的阀值--基本再生数R0,证明了病毒消除平衡点和疾病平衡点的存在性及全局渐近稳定性.     

Isolation of HTLV-transformed B-lymphocyte clone from a patient with HTLV-associated adult T-cell leukaemia

The human T-cell leukaemia/lymphoma virus (HTLV) is an exogenous retrovirus which has been associated with adult T-cell leukaemia/lymphoma (ATL). This malignancy of T lymphocytes is endemic to southern Japan, the West Indies, and to a lesser extent, the Middle East, Central Africa and the southeastern United States. ATL cells from patients of diverse geographical origins have been found to be infected with HTLV-1 (ref.6). HTLV is normally tropic for mature T lymphocytes, especially those expressing the helper-inducer surface antigen phenotype (OKT4 or Leu-3-positive), and the neoplastic T cells infected with HTLV generally express receptors for T-cell growth factor (detected by reactivity with anti-Tac antibody). However, we report here the isolation of a HTLV-infected B-lymphocyte clone from the peripheral blood of a patient with ATL. This clone is cytogenetically normal and is not infected with Epstein-Barr virus (EBV). Co-culture of cells from this clone with cord blood lymphocytes resulted in transmission of HTLV and the immortalization of either T or B lymphocytes. These results suggest that HTLV may be associated with a broader range of host cells than previously recognized.     

HIV病理动力学模型分析

考虑了CD4＋T细胞的全logistic自我繁殖,构造了具有治疗的HIV病理研究模型,研究了解的存在性、正性及稳定性.通过对每个感染T细胞释放的HIV病毒平均数量N的讨论,得到：如果NNcrit,有无病平衡点和地方病平衡点两个平衡点,但此时无病平衡点不稳定,地方病平衡点是局部渐近稳定的.最后通过构造Dulac-Bend...     

The role of evolution in the emergence of infectious diseases

It is unclear when, where and how novel pathogens such as human immunodeficiency virus (HIV), monkeypox and severe acute respiratory syndrome (SARS) will cross the barriers that separate their natural reservoirs from human populations and ignite the epidemic spread of novel infectious diseases. New pathogens are believed to emerge from animal reservoirs when ecological changes increase the pathogen's opportunities to enter the human population and to generate subsequent human-to-human transmission. Effective human-to-human transmission requires that the pathogen's basic reproductive number, R(0), should exceed one, where R(0) is the average number of secondary infections arising from one infected individual in a completely susceptible population. However, an increase in R(0), even when insufficient to generate an epidemic, nonetheless increases the number of subsequently infected individuals. Here we show that, as a consequence of this, the probability of pathogen evolution to R(0) > 1 and subsequent disease emergence can increase markedly.