Reibnegger G, Fuchs D, Hausen A, Werner E R, Dierich M P, Wachter H
Institute for Medicinal Chemistry and Biochemistry, University of Innsbruck, Austria.
Proc Natl Acad Sci U S A. 1987 Oct;84(20):7270-4. doi: 10.1073/pnas.84.20.7270.
The breakdown of the immune system induced by the human immunodeficiency virus might be due to the active immune destruction of human immunodeficiency virus-infected helper T lymphocytes expressing viral antigens. By numerical simulation, we have studied possible consequences that a hypothetical immunodeficiency virus (IDV) may have on the cellular immune response by using a mathematical model. In this model, IDV infects CD4+ (helper) T cells and is actively synthesized by the immunologically activated helper T cells. Infected helper T cells synthesizing IDV express antigenic determinants specific for IDV and trigger a cellular immune response against themselves that is mediated by cytotoxic T cells and cytotoxic macrophages. The dynamic evolution of the model in the case of mixed-type infections with IDV and with another pathogen that evokes a cell-mediated immune response shows strong interactions between both simultaneous infections. The model might be of value to elucidate the dynamics leading to opportunistic infections. Furthermore, a pivotal role for immunological stimulation in the progressive exacerbation of the disease can be demonstrated.
人类免疫缺陷病毒引发的免疫系统崩溃可能是由于表达病毒抗原的人类免疫缺陷病毒感染的辅助性T淋巴细胞受到主动免疫破坏。通过数值模拟,我们使用数学模型研究了一种假设的免疫缺陷病毒(IDV)对细胞免疫反应可能产生的后果。在该模型中,IDV感染CD4 +(辅助性)T细胞,并由免疫激活的辅助性T细胞主动合成。合成IDV的受感染辅助性T细胞表达对IDV特异的抗原决定簇,并引发由细胞毒性T细胞和细胞毒性巨噬细胞介导的针对自身的细胞免疫反应。该模型在IDV与另一种引发细胞介导免疫反应的病原体混合感染情况下的动态演变显示了两种同时感染之间的强烈相互作用。该模型可能有助于阐明导致机会性感染的动态过程。此外,可以证明免疫刺激在疾病进行性加重中起关键作用。