中文摘要：

病毒的传染性因素(Vif ) 被发现为控制 HIV-1 病毒传染性必要。触发它的快降级在 APOBEC 家庭(APO ) 指向细胞的抗病毒的蛋白质并且禁止包装进初生的 virion 的 APO。在现在的学习，我们建议一个数学模型到份量上学习这些典型病毒主人相互作用的细胞内部的动力学。出版试验性的数据的四个集合与模拟结果相比认为模型正当。系统的参数敏感和不安分析证明与 APO 有关的参数对最新综合的 HIV-1 病毒的传染性关键。有趣地，我们发现病毒的结构蛋白质的合成率作呕，要求的数字每初生的 virion 被优化与模型参数的包装 APO，和大部分的最小的水平完成高 virion 生产在一个相对小的范围以内仅仅对病毒有益。而且，在与病毒的蛋白质有关的几个参数的次要的变化梭织，病毒的 RNA 合成的使活跃之物，被发现在合并 Vif 和 APO 上导致像开关的行为。这些调查结果可以为理解 HIV-1 病毒和它的潜伏的高变化率提供新卓见，以及帮助为治疗学的设计识别关键目标。

英文摘要：

The viral infectivity factor （Vif） was found to be essential for controlling HIV-1 virus infectivity. It targets cellular antiviral proteins in APOBEC family （APO） to trigger its fast degradation and inhibits APO packaging into nascent virion. In the present study, we propose a mathematical model to quantitatively study the intracellular dynamics of these typical virus-host interactions. Four sets of published experimental data were compared with simulation results to justify the model. Systematic parameter sensitivity and perturbation analysis showed that parameters related to APO are crucial to the infectivity of newly synthesized HIV-1 virus. Interestingly, we discovered that the synthesis rate of the viral structure protein Gag and the required number per nascent virion are optimized to achieve high virion production with minimal level of packaged APO, and large portion of model parameters are beneficial to virus only within a relatively small range. Furthermore, minor variations in several parameters related to viral protein Tat, the activator of viral RNA synthesis, were found to induce switch-like behaviors on both incorporated Vif and APO. These findings may provide new insights for understanding the high mutation rate of HIV-1 virus and its latency, as well as help identify key targets for therapeutic design.