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首页> 外文会议>BIOMAT 2011 >MATHEMATICAL MODELLING OF THE INTERACTION BETWEEN Mycobacterium Tuberculosis INFECTION AND CELLULAR IMMUNE RESPONSE
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MATHEMATICAL MODELLING OF THE INTERACTION BETWEEN Mycobacterium Tuberculosis INFECTION AND CELLULAR IMMUNE RESPONSE

机译：结核分枝杆菌感染与细胞免疫应答相互作用的数学建模

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In general, cellular immune response results in the suppression of mycobacterial infection, but does not completely eradicate it. This is the reason why the majority of cases (95%) limits proliferation of the bacilli and produces a long-lasting partial immunity, and 5% of infected individuals develop early progressive disease that occurs within 2-5 years of infection. One of the characteristics of Mycobacterium infection is the replication of the bacteria inside of alveolar macrophages. For this reason 5% of asymptomatic individuals have late disease, which is caused by endogenous reactivation as long as several decades after infection. We develop a simple mathematical model that describes the interaction between Mycobacterium tuberculosis and cellular immune response. The risk of tuberculosis reactivation is determined by granulomas formation on one side and cellular immune response to phagocytize bacteria and to destroy granuloma on other side. The model is analyzed in the initial phase of mycobacterial infection, and an associated risk of tuberculosis among tobacco smokers is established.
机译：一般来说，细胞免疫反应导致抑制分枝杆菌感染，但并不完全消除它。这就是为什么大多数病例（95％）限制肉芽碱增殖并产生持久的部分免疫力，5％的受感染的个体发育早期进展疾病发生在感染后2 - 5年内的早期疾病。分枝杆菌感染的特征之一是肺泡巨噬细胞内部的复制。因此，5％的无症状的个体具有晚期疾病，这是由于感染后几十年的内源再活化引起的。我们开发了一种简单的数学模型，描述了结核分枝杆菌和细胞免疫应答之间的相互作用。结核病重新激活的风险由肉芽肿形成的一侧和细胞免疫反应对吞噬细菌的反应和破坏肉芽肿在另一边破坏肉芽肿。该模型在分枝杆菌感染的初始阶段分析，建立了烟草吸烟者之间结核病的相关风险。

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