Hraba T, Dolezal J, Celikovský S
Institute of Molecular Genetics, Czećhoslovak Academy of Sciences, Prague.
Immunobiology. 1990 Aug;181(1):108-18. doi: 10.1016/S0171-2985(11)80169-5.
The previously suggested mathematical model of CD4+ lymphocyte depletion in HIV-infected individuals is analyzed and further developed. The model assumes that CD4+ lymphocyte depletion is caused by HIV products. Fairly good simulation of CD4+ lymphocyte dynamics is obtained, when limitation of HIV growth by specific cytotoxic T cells is included in the model. As it is probable that the substantial decrease of CD4+ lymphocytes, this type of influx control mechanism is also included in the model. It is shown that the simulated CD4+ lymphocyte dynamics agree with the observed data, analogously as in the earlier considered case of the constant influx. Moreover, the depleting effect of HIV products on mature and/or immature CD4+ lymphocytes is analyzed by the model. Also, another modification of the model assuming that CD4+ lymphocyte depletion is due to their destruction by cytotoxic T cells specific for HIV antigens, gives simulation results comparable to those obtained by the original version of the model, where the mechanism of the depletion is not specified.
对先前提出的关于HIV感染个体中CD4 +淋巴细胞耗竭的数学模型进行了分析并进一步完善。该模型假定CD4 +淋巴细胞耗竭是由HIV产物引起的。当模型中纳入特异性细胞毒性T细胞对HIV生长的限制时，可获得对CD4 +淋巴细胞动态变化的相当良好的模拟。由于CD4 +淋巴细胞很可能会大幅减少，这种类型的流入控制机制也被纳入模型。结果表明，模拟的CD4 +淋巴细胞动态变化与观察数据相符，这与早期考虑的恒定流入情况类似。此外，该模型分析了HIV产物对成熟和/或未成熟CD4 +淋巴细胞的耗竭作用。另外，对模型进行的另一种修改假定CD4 +淋巴细胞耗竭是由于针对HIV抗原的细胞毒性T细胞对它们的破坏，其模拟结果与未明确耗竭机制的原始模型版本所获得的结果相当。
