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Acute hepatitis B virus infection model within the host incorporating immune cells and cytokine responses.
Theory in Biosciences ( IF 1.3 ) Pub Date : 2019-10-24 , DOI: 10.1007/s12064-019-00305-2
Edna Chilenje Manda 1 , Faraimunashe Chirove 1, 2
Affiliation  

We formulate and analyze a within-host hepatitis B viral mathematical model for hepatitis B in the acute phase of infection. The model incorporates hepatocytes, hepatitis B virus, immune system cells and cytokine dynamics using a system of ordinary differential equations. We use the model to demonstrate the trends of the hepatitis B infection qualitatively without the effects of immune cells and cytokines. Using these trends, we tested the effects of incorporating the immune cells only and immune cells with cytokine responses at low and high inhibitions on the hepatitis B virus infection. Our results showed that it is impossible to have the immune cells work independently from cytokines when there is an acute hepatitis B virus infection. Therefore, our results suggest that incorporating immune cells and cytokine dynamics in the acute hepatitis B virus infection stage delays infection in the hepatocytes and excluding such dynamics speeds up infection during this phase. Results from this study are useful in developing strategies for control of hepatocellular carcinoma which is caused by hepatitis B virus infection.

中文翻译:

宿主内包含免疫细胞和细胞因子反应的急性乙型肝炎病毒感染模型。

我们在感染的急性期制定并分析了宿主内的乙型肝炎病毒数学模型。该模型使用常微分方程组整合了肝细胞,乙型肝炎病毒,免疫系统细胞和细胞因子动力学。我们使用该模型定性地证明了乙型肝炎感染的趋势,而没有免疫细胞和细胞因子的影响。利用这些趋势,我们测试了将免疫细胞和具有细胞因子应答的免疫细胞以低和高抑制率并入乙型肝炎病毒感染的效果。我们的结果表明,当急性乙型肝炎病毒感染时,不可能让免疫细胞独立于细胞因子发挥作用。因此,我们的结果表明,在急性乙型肝炎病毒感染阶段纳入免疫细胞和细胞因子动力学会延迟肝细胞的感染,而排除这种动力学会加快此阶段的感染。这项研究的结果可用于开发控制由乙型肝炎病毒感染引起的肝细胞癌的策略。
更新日期:2019-10-24
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