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A mathematical study on immune activation and related dynamics in HIV infection

机译:HIV感染中免疫激活和相关动力学的数学研究

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Over decades, mathematical models have been applied successfully to the investigation of HIV dynamics. However, few of these investigations are able to explain the observation that host (CD4+ T) cell counts reduce, while viral load increases as the infection progresses. Various clinical studies of HIV infection have suggested that high T-cell activation levels are positively correlated with rapid disease development in untreated patients. This activation might be a major reason for the depletion of CD4+ T cells observed in most cases of long term untreated HIV infection. In this paper, we use a simple mathematical model to investigate immune activation and its role in HIV infection. Under reasonable assumptions relating to various HIV infection constants, we show that enhanced activation and reduced reversion in the immune system do result in depleted CD4+ T cell count. We further show that this process is robust to parameter variations. An extended model including viral dynamics illustrates the effects of immune activation on viral persistence and immune response. Simulations are given to verify the theoretical analysis.
机译:数十年来,数学模型已成功应用于艾滋病毒动力学研究。但是,这些研究很少能够解释观察到的结果,即宿主(CD4 + T)细胞数量减少,而病毒载量随着感染的进展而增加。 HIV感染的各种临床研究表明,高T细胞活化水平与未经治疗的患者疾病的快速发展呈正相关。在大多数长期未治疗的HIV感染病例中,这种激活可能是导致CD4 + T细胞耗竭的主要原因。在本文中,我们使用简单的数学模型来研究免疫激活及其在HIV感染中的作用。在与各种HIV感染常数有关的合理假设下,我们表明免疫系统中增强的激活和减少的逆转确实导致CD4 + T细胞计数减少。我们进一步表明,该过程对于参数变化具有鲁棒性。包含病毒动力学的扩展模型说明了免疫激活对病毒持久性和免疫反应的影响。仿真结果验证了理论分析的正确性。

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