Cancer Research Center, Qatar Biomedical Research Institute (QBRI), Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Doha 34110, Qatar.
College of Health & Life Sciences, Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Doha 34110, Qatar.
Genes (Basel). 2020 Jul 7;11(7):760. doi: 10.3390/genes11070760.
The global spread of COVID-19, caused by pathogenic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) underscores the need for an imminent response from medical research communities to better understand this rapidly spreading infection. Employing multiple bioinformatics and computational pipelines on transcriptome data from primary normal human bronchial epithelial cells (NHBE) during SARS-CoV-2 infection revealed activation of several mechanistic networks, including those involved in immunoglobulin G (IgG) and interferon lambda (IFNL) in host cells. Induction of acute inflammatory response and activation of tumor necrosis factor (TNF) was prominent in SARS-CoV-2 infected NHBE cells. Additionally, disease and functional analysis employing ingenuity pathway analysis (IPA) revealed activation of functional categories related to cell death, while those associated with viral infection and replication were suppressed. Several interferon (IFN) responsive gene targets (IRF9, IFIT1, IFIT2, IFIT3, IFITM1, MX1, OAS2, OAS3, IFI44 and IFI44L) were highly upregulated in SARS-CoV-2 infected NBHE cell, implying activation of antiviral IFN innate response. Gene ontology and functional annotation of differently expressed genes in patient lung tissues with COVID-19 revealed activation of antiviral response as the hallmark. Mechanistic network analysis in IPA identified 14 common activated, and 9 common suppressed networks in patient tissue, as well as in the NHBE cell model, suggesting a plausible role for these upstream regulator networks in the pathogenesis of COVID-19. Our data revealed expression of several viral proteins in vitro and in patient-derived tissue, while several host-derived long noncoding RNAs (lncRNAs) were identified. Our data highlights activation of IFN response as the main hallmark associated with SARS-CoV-2 infection in vitro and in human, and identified several differentially expressed lncRNAs during the course of infection, which could serve as disease biomarkers, while their precise role in the host response to SARS-CoV-2 remains to be investigated.
新型冠状病毒病(COVID-19)的全球传播是由致病性严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)引起的,这突显出医疗研究界需要立即做出反应,以便更好地了解这种迅速传播的感染。对 SARS-CoV-2 感染期间原代正常人支气管上皮细胞(NHBE)的转录组数据进行多次生物信息学和计算分析,揭示了几个机制网络的激活,包括宿主细胞中免疫球蛋白 G(IgG)和干扰素 lambda(IFNL)的网络。在 SARS-CoV-2 感染的 NHBE 细胞中,急性炎症反应和肿瘤坏死因子(TNF)的激活是显著的。此外,采用 ingenuity pathway analysis(IPA)进行疾病和功能分析,揭示了与细胞死亡相关的功能类别被激活,而与病毒感染和复制相关的功能类别被抑制。SARS-CoV-2 感染 NBHE 细胞中几个干扰素(IFN)反应基因靶标(IRF9、IFIT1、IFIT2、IFIT3、IFITM1、MX1、OAS2、OAS3、IFI44 和 IFI44L)高度上调,暗示抗病毒 IFN 固有反应的激活。COVID-19 患者肺组织中差异表达基因的基因本体和功能注释揭示了抗病毒反应的激活是其特征。IPA 中的机制网络分析确定了患者组织以及 NHBE 细胞模型中 14 个共同激活和 9 个共同抑制网络,这表明这些上游调节网络在 COVID-19 发病机制中可能具有一定作用。我们的数据揭示了几种病毒蛋白在体外和患者衍生组织中的表达,同时鉴定了几种宿主衍生的长非编码 RNA(lncRNA)。我们的数据强调了 IFN 反应的激活是 SARS-CoV-2 体外和人类感染的主要特征,并确定了感染过程中几个差异表达的 lncRNA,它们可以作为疾病生物标志物,而它们在宿主对 SARS-CoV-2 反应中的精确作用仍有待研究。