Department of Biological Sciences, University of the Sciences, Philadelphia, Pennsylvania, United States of America.
Current institution - Department of Infectious Diseases and Vaccines, MRL, Merck & Co., Inc., West Point, Pennsylvania, United States of America.
PLoS One. 2020 Mar 25;15(3):e0230563. doi: 10.1371/journal.pone.0230563. eCollection 2020.
Despite antiretroviral therapy human immunodeficiency virus type-1 (HIV-1) infection results in neuroinflammation of the central nervous system that can cause HIV-associated neurocognitive disorders (HAND). The molecular mechanisms involved in the development of HAND are unclear, however, they are likely due to both direct and indirect consequences of HIV-1 infection and inflammation of the central nervous system. Additionally, opioid abuse in infected individuals has the potential to exacerbate HIV-comorbidities, such as HAND. Although restricted for productive HIV replication, astrocytes (comprising 40-70% of all brain cells) likely play a significant role in neuropathogenesis in infected individuals due to the production and response of viral proteins. The HIV-1 protein Tat is critical for viral transcription, causes neuroinflammation, and can be secreted from infected cells to affect uninfected bystander cells. The Wnt/β-catenin signaling cascade plays an integral role in restricting HIV-1 infection in part by negatively regulating HIV-1 Tat function. Conversely, Tat can overcome this negative regulation and inhibit β-catenin signaling by sequestering the critical transcription factor TCF-4 from binding to β-catenin. Here, we aimed to explore how opiate exposure affects Tat-mediated suppression of β-catenin in astrocytes and the downstream modulation of neuroinflammatory genes. We observed that morphine can potentiate Tat suppression of β-catenin activity in human astrocytes. In contrast, Tat mutants deficient in secretion, and lacking neurotoxic effects, do not affect β-catenin activity in the presence or absence of morphine. Finally, morphine treatment of astrocytes was sufficient to reduce the expression of genes involved in neuroinflammation. Examining the molecular mechanisms of how HIV-1 infection and opiate exposure exacerbate neuroinflammation may help us inform or predict disease progression prior to HAND development.
尽管抗逆转录病毒疗法可抑制人类免疫缺陷病毒 1 型(HIV-1)感染,但仍会导致中枢神经系统的神经炎症,从而引起与 HIV 相关的认知障碍(HAND)。HAND 发生的分子机制尚不清楚,但可能是由于 HIV-1 感染和中枢神经系统炎症的直接和间接后果所致。此外,感染个体的阿片类药物滥用有可能使 HAND 等 HIV 合并症恶化。尽管 HIV-1 受到限制而无法进行有效复制,但星形胶质细胞(约占所有脑细胞的 40-70%)由于病毒蛋白的产生和反应,可能在感染个体的神经发病机制中发挥重要作用。HIV-1 蛋白 Tat 对于病毒转录至关重要,可引起神经炎症,并可从受感染的细胞中分泌出来,从而影响未受感染的旁观者细胞。Wnt/β-连环蛋白信号级联反应在限制 HIV-1 感染中起着重要作用,部分原因是通过负调控 HIV-1 Tat 功能来实现的。相反,Tat 可以通过将关键转录因子 TCF-4 与 β-连环蛋白结合来阻止这种负调控并抑制 β-连环蛋白信号。在这里,我们旨在探讨阿片类药物暴露如何影响 Tat 介导的星形胶质细胞中 β-连环蛋白的抑制作用,以及对神经炎症基因的下游调节。我们观察到吗啡可以增强 Tat 对人星形胶质细胞中 β-连环蛋白活性的抑制作用。相反,缺乏分泌和神经毒性作用的 Tat 突变体在有无吗啡的情况下均不影响 β-连环蛋白活性。最后,吗啡处理星形胶质细胞足以降低与神经炎症相关的基因的表达。研究 HIV-1 感染和阿片类药物暴露如何加重神经炎症的分子机制,可能有助于我们在 HAND 发展之前了解或预测疾病的进展。