Drugs of abuse, such as opiates, have been widely associated with the enhancement of HIV replication, the acceleration of disease progression, and severe neuropathogenesis. Specifically, the presence of drugs of abuse (morphine) switches target cells (CD4\(^+\) T cells) from lower-to-higher susceptibility to HIV infection. The effect of such switching behaviors on viral dynamics may be altered due to the intracellular delay (the replication time between viral entry into a target cell and the production of new viruses by the infected cell). In this study, we develop, for the first time, a viral dynamics model that includes an intracellular delay under the conditioning of drugs of abuse. We parameterize the model using experimental data from simian immunodeficiency virus infection of morphine-addicted macaques. Results from thorough mathematical analyses and numerical simulations of our model show that the intracellular delay can play a significant role in HIV dynamics under the conditioning of drugs of abuse, particularly during the acute phase of infection. Our model and the related results provide new insights into the HIV dynamics and may help develop strategies to control HIV infections in drug abusers.

滥用药物，如阿片类药物，与 HIV 复制的增强、疾病进展的加速和严重的神经发病机制密切相关。具体来说，滥用药物（吗啡）的存在会切换靶细胞（CD4 \(^+\)T 细胞）对 HIV 感染的易感性从低到高。由于细胞内延迟（病毒进入靶细胞和受感染细胞产生新病毒之间的复制时间），这种转换行为对病毒动力学的影响可能会改变。在这项研究中，我们首次开发了一种病毒动力学模型，其中包括在滥用药物条件下的细胞内延迟。我们使用来自对吗啡成瘾的猕猴的猿猴免疫缺陷病毒感染的实验数据来参数化模型。我们模型的彻底数学分析和数值模拟结果表明，在滥用药物的条件下，尤其是在感染的急性期，细胞内延迟可以在 HIV 动力学中发挥重要作用。