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首页> 外文期刊>IEEE/ACM transactions on computational biology and bioinformatics >Systematic Analysis of the Mechanisms of Virus-Triggered Type I IFN Signaling Pathways through Mathematical Modeling
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Systematic Analysis of the Mechanisms of Virus-Triggered Type I IFN Signaling Pathways through Mathematical Modeling

机译：通过数学建模对病毒触发的I型IFN信号通路机制的系统分析

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摘要

Based on biological experimental data, we developed a mathematical model of the virus-triggered signaling pathways that lead to induction of type I IFNs and systematically analyzed the mechanisms of the cellular antiviral innate immune responses, including the negative feedback regulation of ISG56 and the positive feedback regulation of IFNs. We found that the time between 5 and 48 hours after viral infection is vital for the control and/or elimination of the virus from the host cells and demonstrated that the ISG56-induced inhibition of MITA activation is stronger than the ISG56-induced inhibition of TBK1 activation. The global parameter sensitivity analysis suggests that the positive feedback regulation of IFNs is very important in the innate antiviral system. Furthermore, the robustness of the innate immune signaling network was demonstrated using a new robustness index. These results can help us understand the mechanisms of the virus-induced innate immune response at a system level and provide instruction for further biological experiments.
机译：基于生物学实验数据，我们开发了导致I型干扰素诱导的病毒触发信号通路的数学模型，并系统分析了细胞抗病毒先天免疫应答的机制，包括ISG56的负反馈调节和正反馈干扰素的调节。我们发现病毒感染后5到48小时之间的时间对于控制和/或从宿主细胞中消除病毒至关重要，并证明ISG56诱导的MITA激活抑制作用强于ISG56诱导的TBK1抑制作用激活。全局参数敏感性分析表明，IFNs的正反馈调节在先天抗病毒系统中非常重要。此外，使用新的鲁棒性指数证明了先天免疫信号网络的鲁棒性。这些结果可以帮助我们在系统水平上理解病毒诱导的先天免疫应答的机制，并为进一步的生物学实验提供指导。

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