Department of Theoretical Microelectronics, A.F. Ioffe Physical Technical Institute, 26 Polytechnicheskaya St, St. Petersburg 194021, Russia.
J Theor Biol. 2010 Apr 7;263(3):369-84. doi: 10.1016/j.jtbi.2009.11.003. Epub 2009 Nov 12.
Recently, we developed a mathematical model of interaction between the HIV and the immune system to match various dynamic experiments carried out in HIV-infected humans and SIV-infected macaques. The model includes helper cell-dependent and helper cell-independent cytotoxic lymphocytes (CTLs) and predicts two stable steady states, a state with a high virus load and few helper cells, and another state with a low virus load and many helper cells. Here we upgrade the model to take into account recent reports on the link between the activation status of infected cells and their ability to produce virus, the effect of helper cells at the time of priming on CTL differentiation, and virus dynamics in unvaccinated macaques with a broad genetic background acutely infected with SIVmac251. We also discuss in detail the experimental justification of the CTL block and the robustness of model predictions with respect to the hypothesis of two CTL subtypes.
最近，我们开发了一个 HIV 与免疫系统相互作用的数学模型，以匹配在 HIV 感染人类和 SIV 感染恒河猴中进行的各种动态实验。该模型包括辅助细胞依赖性和辅助细胞非依赖性细胞毒性 T 淋巴细胞（CTL），并预测了两种稳定的稳态，一种是病毒载量高、辅助细胞少的状态，另一种是病毒载量低、辅助细胞多的状态。在这里，我们升级了该模型，以考虑到最近关于感染细胞的激活状态与其产生病毒能力之间的联系、在初始阶段辅助细胞对 CTL 分化的影响，以及在急性感染 SIVmac251 的具有广泛遗传背景的未接种疫苗恒河猴中病毒动力学的相关报告。我们还详细讨论了 CTL 阻断的实验依据，以及该模型预测对两种 CTL 亚型假设的稳健性。
