Hraba T, Dolezal J
Institute of Molecular Genetics, Academy of Sciences of the Czech Republic, Praha.
Folia Biol (Praha). 1995;41(6):304-18.
The previously developed mathematical model of CD4+ lymphocyte dynamics in HIV infection incorporated a homeostatic mechanism regulating production of both CD4+ and CD8+ lymphocytes. The model simulated the CD4+ lymphocyte dynamics well, but simulation of CD8+ lymphocyte values was not satisfactory, because simulated numbers of these cells increased even at later stages of infection, when no further increase was observed in infected individuals. Modifications of the model were attempted to obtain better simulation results assuming the influence of HIV infection on CD8+ lymphocyte maturation. Satisfactory results were obtained, if the influx of immature CD4+ and CD8+ lymphocytes was constrained by HIV infection. This modified version was then used for simulation of the anti-CD8 antibody administration effect in HIV-infected persons.
先前开发的HIV感染中CD4+淋巴细胞动力学数学模型纳入了一种调节CD4+和CD8+淋巴细胞生成的稳态机制。该模型能很好地模拟CD4+淋巴细胞动力学,但对CD8+淋巴细胞值的模拟并不令人满意,因为这些细胞的模拟数量即使在感染后期也会增加,而在感染个体中并未观察到进一步增加。假设HIV感染对CD8+淋巴细胞成熟有影响,尝试对模型进行修改以获得更好的模拟结果。如果未成熟的CD4+和CD8+淋巴细胞的流入受到HIV感染的限制,就能获得满意的结果。然后将这个修改后的版本用于模拟HIV感染者中抗CD8抗体给药的效果。