HIV-1的表型间变异与免疫因子相互作用的动力学模型

该文建立了一个描述两种不同的 HIV-1 表型与细胞因子相互作用的动力学模型. 作者用K_m单调系统理论研究了 HIV-1 中两种不同表型:噬巨嗜细胞型 (NSI) 和嗜淋巴细胞型 (SI) 与两种在HIV感染过程中的重要指标性细胞因子:IL-2 和 CAF的发展趋势. 在 HIV-1 感染过程中,两种细胞表型与两种细胞因子之间形成了一种负反馈环. 用 Hill 函数表达这种负反馈作用. 结果表明模型的平衡态的数量为奇数个,它们之间满足一种K_m 偏序,并且第奇数个平衡态是渐近稳定的,而第偶数平衡态是不稳定的. 此外还得到了各个平衡态的吸引域. 其生物学的意义为:即使系统存在较低水平的平衡态, 感染后的病毒载量仍会趋向于一个较高的水平. 这个结论和临床研究的发现是一致的.

Modeling the Interactions between the HIV-1 Phenotypes and the Cytokines

In this paper, the authors present a model illustrateing the interactions between the two HIV-1 phenotypes and cytokines. By introducing the important cytokines, IL-2 and CAF, in the HIV-1 dynamics model, the authors study the evolution of the two different HIV-1 phenotypes: the M-tropic (NSI) and the T-cell-tropic (SI). Using the type Km monotone system theory, the authors obtain two results. First, the number of steady states of the system is odd, the odd indexed equilibria are asymptotically stable, and the even ones are unstable. Secondly, some detailed information about the bases of attraction of these steady states has been obtained. These results indicate that the two phenotypes will coexist in the infected patient for long time. Moreover, all these results can be explained by the pathogenesis of AIDS and are consistent with the results of clinical studies.