Mechanisms for Cell-to-cell and Cell-free Spread of HIV-1 in Cellular Automata Models

P. Giabbanelli, Cole Freeman, Joshua A. Devita, Nicholas Rosso, Z. Brumme
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引用次数: 14

Abstract

Several discrete simulation models have been created to study the spread of human immunodeficiency virus type 1 (HIV-1) within a human body. This is motivated both by the prevalence of the virus, and by the possibility of asking questions in simulations that would be unethical to test in trials. Among discrete simulation techniques, cellular automata (CA) have been particularly used in HIV-1 research. CA commonly assume that a cell is almost exclusively infected by neighboring cells (i.e., cell-to-cell transmission), and that more distal cells (i.e., cell-free transmission) have an extremely small probability to transmit the disease. The mechanisms are more nuanced in recent biological research, suggesting that cell-to-cell transmission may account for about 60% of all transmissions. We show that a representative sample of five previously validated CA models of HIV-1 can all be altered (by changing neighborhood structures and infection probabilities) to produce a realistic share of cell-to-cell and cell-free viral transmissions. Increasing the realism for modes of transmission, however, has mixed consequences on preserving the models' validity: their predictions at 600 weeks are generally unchanged, but viral dynamics are markedly different. We offer several suggestions to create CA models of HIV-1 with realistic infections and plausible viral dynamics.
细胞自动机模型中HIV-1细胞间和无细胞传播的机制
已经建立了几个离散的模拟模型来研究人类免疫缺陷病毒1型(HIV-1)在人体内的传播。这既是由于病毒的流行,也是由于在模拟中提出问题的可能性,而在试验中进行测试是不道德的。在离散模拟技术中,细胞自动机(CA)在HIV-1研究中得到了特别的应用。CA通常假设一个细胞几乎完全被邻近细胞感染(即细胞间传播),而更远的细胞(即无细胞传播)传播疾病的可能性极小。在最近的生物学研究中,这种机制更加微妙,表明细胞间传播可能占所有传播的60%左右。我们表明,五个先前验证的HIV-1 CA模型的代表性样本都可以被改变(通过改变邻域结构和感染概率),以产生细胞间和无细胞病毒传播的实际份额。然而,增加传播模式的真实性对保持模型的有效性产生了复杂的后果:它们在600周时的预测通常不变,但病毒动态明显不同。我们提出了一些建议,以创建具有现实感染和似是而非的病毒动力学的HIV-1的CA模型。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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