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首页> 外文期刊>Science World Journal >HIV/AIDS-INVIVO MODEL WITH THE ROLES OF CTL IMMUNE CELLS AND ANTIRETROVIRAL THERAPHY
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HIV/AIDS-INVIVO MODEL WITH THE ROLES OF CTL IMMUNE CELLS AND ANTIRETROVIRAL THERAPHY

机译:具有CTL免疫细胞作用和抗病毒治疗的HIV / AIDS-INVIVO模型

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In this work, we formulated a mathematical model to study the interaction between HIV/AIDS and Cluster of Differentiation 4 cells (CD4+T), incorporating the roles of Cytotoxic T- lymphocytes (CTLs) cells and antiretroviral therapy. The proliferation of CD4+T cells was considered to follow the logistic growth pattern. The presence of HIV in the CD4+T cells stimulates the recruitment of CD4+T and CTL cells. The recruitment of uninfected CD4+T and CTL immune cells fall purely as an exponential function of time in the presence of HIV. The basic reproduction number was obtained using the next generation matrix method. We adopted the Jacobian stability criterion and the Lyaponuv second method of stability to establish the local and global stabilities of the equilibrium states and show that HIV can be eliminated from CD4+T cells when ?but will continue to persist within CD4+T cells when . Early medication therapy was observed to reduce viral load and increase the number of CTL cells, while CD4+T cells is kept above the AIDS bar. A high initial viral load was noticed to induce rapid decline in the number of CD4+T cells. To keep a healthy system, we recommended that the CTL and uninfected CD4+T cells population should be maintained by reducing viral load through early medication therapy and cloning of CTL cells within infected human, which fights and kills infected cells.
机译:在这项工作中,我们建立了一个数学模型来研究HIV / AIDS与分化4细胞簇(CD4 + T)之间的相互作用,并结合了细胞毒性T淋巴细胞(CTL)细胞和抗逆转录病毒疗法的作用。 CD4 + T细胞的增殖被认为遵循逻辑生长模式。 CD4 + T细胞中HIV的存在会刺激CD4 + T和CTL细胞的募集。在HIV存在下,未感染的CD4 + T和CTL免疫细胞的募集纯粹是时间的指数函数。基本再现数是使用下一代矩阵方法获得的。我们采用雅可比稳定性准则和Lyaponuv第二种稳定性方法建立了平衡态的局部和全局稳定性,并表明当时HIV可以从CD4 + T细胞中清除,但当时将继续存在于CD4 + T细胞中。观察到早期药物治疗可减少病毒载量并增加CTL细胞的数量,而CD4 + T细胞则保持在AIDS上方。注意到高的初始病毒载量可诱导CD4 + T细胞数量迅速下降。为了保持系统健康,我们建议通过早期药物治疗和克隆感染的人体内的CTL细胞来减少病毒载量,从而维持CTL和未感染的CD4 + T细胞的数量,从而对抗和杀死感染的细胞。

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