Gene Expression Profiling Reveals the Shared and Distinct Transcriptional Signatures in Human Lung Epithelial Cells Infected With SARS-CoV-2, MERS-CoV, or SARS-CoV: Potential Implications in Cardiovascular Complications of COVID-19.
Gene Expression Profiling Reveals the Shared and Distinct Transcriptional Signatures in Human Lung Epithelial Cells Infected With SARS-CoV-2, MERS-CoV, or SARS-CoV: Potential Implications in Cardiovascular Complications of COVID-19.
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DOI：
10.3389/fcvm.2020.623012
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发表时间：
2020
影响因子：
3.6
通讯作者：
Aikawa M
中科院分区：
文献类型：
--
作者：
Jha PK;Vijay A;Halu A;Uchida S;Aikawa M
严重急性呼吸综合征冠状病毒2 （SARS-CoV-2）是目前全球大流行的冠状病毒病2019 （COVID-19）的致病病毒。SARS- cov -2属于被称为冠状病毒的单链RNA病毒家族，包括分别引起中东呼吸综合征（MERS）和严重急性呼吸综合征（SARS）的MERS- cov和SARS- cov。这些冠状病毒引起轻度至重度上呼吸道疾病的方式是相关的。本研究对来自gene expression Omnibus的公开基因表达数据集进行了无偏分析，以了解感染SARS-CoV-2的人肺上皮细胞相对于MERS-CoV或SARS-CoV的共同和独特转录特征。一个主要目标是在这三种冠状病毒中发现对SARS-CoV-2的独特细胞反应。分析三个数据集共享的差异表达基因（DEGs），得出一组17个基因，提示SARS-CoV-2中与急性炎症反应相关的基因（TNF、IL32、IL1A、CXCL1和CXCL3）的表达较低。这种对SARS-CoV-2的抑制转录反应可能导致病毒复制时间延长，导致严重的肺损伤。对SARS- cov -2感染独特基因的下游分析显示，与细胞凋亡（NRP1、FOXO1、TP53INP1、CSF2和NLRP1）、凝血（F3、PROS1、ITGB3和TFPI2）和血管功能（VAV3、TYMP、TCF4和NR2F2）相关的基因发生了变化，这可能是COVID-19比MERS和SARS更多系统性心血管并发症的原因。该研究发现了一组新的转录组特征，这些特征是SARS-CoV-2感染所特有的，并且是三种冠状病毒共有的，这可能为开发COVID-19预后或治疗工具的初步工作提供指导。
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative virus for the current global pandemic known as coronavirus disease 2019 (COVID-19). SARS-CoV-2 belongs to the family of single-stranded RNA viruses known as coronaviruses, including the MERS-CoV and SARS-CoV that cause Middle East respiratory syndrome (MERS) and severe acute respiratory syndrome (SARS), respectively. These coronaviruses are associated in the way that they cause mild to severe upper respiratory tract illness. This study has used an unbiased analysis of publicly available gene expression datasets from Gene Expression Omnibus to understand the shared and unique transcriptional signatures of human lung epithelial cells infected with SARS-CoV-2 relative to MERS-CoV or SARS-CoV. A major goal was to discover unique cellular responses to SARS-CoV-2 among these three coronaviruses. Analyzing differentially expressed genes (DEGs) shared by the three datasets led to a set of 17 genes, suggesting the lower expression of genes related to acute inflammatory response (TNF, IL32, IL1A, CXCL1, and CXCL3) in SARS-CoV-2. This subdued transcriptional response to SARS-CoV-2 may cause prolonged viral replication, leading to severe lung damage. Downstream analysis of unique DEGs of SARS-CoV-2 infection revealed changes in genes related to apoptosis (NRP1, FOXO1, TP53INP1, CSF2, and NLRP1), coagulation (F3, PROS1, ITGB3, and TFPI2), and vascular function (VAV3, TYMP, TCF4, and NR2F2), which may contribute to more systemic cardiovascular complications of COVID-19 than MERS and SARS. The study has uncovered a novel set of transcriptomic signatures unique to SARS-CoV-2 infection and shared by three coronaviruses, which may guide the initial efforts in the development of prognostic or therapeutic tools for COVID-19.
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