Abstract：
Simian immunodeficiency virus (SIV) infection in rhesus macaques (Macaca mulatta) can lead to the development of SIV encephalitis (SIVE), which is closely related to human immunodeficiency virus (HIV)-induced dementia.
This was done by analyzing SIV and SIVE encephalitis in infected M. mulatta hippocampus samples from two microarray data sets, identifying two groups of common differentially expressed genes and predicting associated protein interactions.
We found that eight genes-MX1, B2M, IFIT1, TYMP, STAT1, IFI44, ISG15, and IFI27-affected the negative regulation of biological processes, hepatitis C and Epstein-Barr viral infection, and the toll-like receptor signaling pathway, which mediate the development of encephalitis after SIV infection. In particular, STAT1 played a central role in the process by regulating biopathological changes during the development of SIVE.
These findings provide a new theoretical basis for the treatment of encephalopathy after HIV infection by targeting STAT1.
This was done by analyzing SIV and SIVE encephalitis in infected M. mulatta hippocampus samples from two microarray data sets, identifying two groups of common differentially expressed genes and predicting associated protein interactions.
We found that eight genes-MX1, B2M, IFIT1, TYMP, STAT1, IFI44, ISG15, and IFI27-affected the negative regulation of biological processes, hepatitis C and Epstein-Barr viral infection, and the toll-like receptor signaling pathway, which mediate the development of encephalitis after SIV infection. In particular, STAT1 played a central role in the process by regulating biopathological changes during the development of SIVE.
These findings provide a new theoretical basis for the treatment of encephalopathy after HIV infection by targeting STAT1.
摘要：
背景：猕猴（猕猴）中的猿猴免疫缺陷病毒（SIV）感染可导致SIV脑炎（SIVE）的发展，与人类免疫缺陷病毒（HIV）引起的痴呆密切相关。
方法：这是通过分析来自两个微阵列数据集的受感染的M.mulatta海马样本中的SIV和SIVE脑炎来完成的，确定两组常见的差异表达基因并预测相关的蛋白质相互作用。
结果：我们发现八个基因-MX1，B2M，IFIT1,TYMP,STAT1，IFI44，ISG15和IFI27-影响生物过程的负调控，丙型肝炎和EB病毒感染，和toll样受体信号通路，介导SIV感染后脑炎的发展。特别是,STAT1通过调节SIVE发育过程中的生物病理学变化在该过程中起着核心作用。
结论：这些发现为靶向STAT1治疗HIV感染后脑病提供了新的理论依据。
方法：这是通过分析来自两个微阵列数据集的受感染的M.mulatta海马样本中的SIV和SIVE脑炎来完成的，确定两组常见的差异表达基因并预测相关的蛋白质相互作用。
结果：我们发现八个基因-MX1，B2M，IFIT1,TYMP,STAT1，IFI44，ISG15和IFI27-影响生物过程的负调控，丙型肝炎和EB病毒感染，和toll样受体信号通路，介导SIV感染后脑炎的发展。特别是,STAT1通过调节SIVE发育过程中的生物病理学变化在该过程中起着核心作用。
结论：这些发现为靶向STAT1治疗HIV感染后脑病提供了新的理论依据。
