Abstract
Coronavirus disease 2019 (COVID-19) is acutely infectious pneumonia. Currently, the specific causes and treatment targets of COVID-19 are still unclear. Herein, comprehensive bioinformatics methods were employed to analyze the hub genes in COVID-19 and tried to reveal its potential mechanisms. First of all, 34 groups of COVID-19 lung tissues and 17 other diseases' lung tissues were selected from the GSE151764 gene expression profile for research. According to the analysis of the DEGs (differentially expressed genes) in the samples using the limma software package, 84 upregulated DEGs and 46 downregulated DEGs were obtained. Later, by the Database for Annotation, Visualization, and Integrated Discovery (DAVID), they were enriched in the Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. It was found that the upregulated DEGs were enriched in the type I interferon signaling pathway, AGE-RAGE signaling pathway in diabetic complications, coronavirus disease, etc. Downregulated DEGs were in cellular response to cytokine stimulus, IL-17 signaling pathway, FoxO signaling pathway, etc. Then, based on GSEA, the enrichment of the gene set in the sample was analyzed in the GO terms, and the gene set was enriched in the positive regulation of myeloid leukocyte cytokine production involved in immune response, programmed necrotic cell death, translesion synthesis, necroptotic process, and condensed nuclear chromosome. Finally, with the help of STRING tools, the PPI (protein-protein interaction) network diagrams of DEGs were constructed. With degree ≥13 as the cutoff degree, 3 upregulated hub genes (ISG15, FN1, and HLA-G) and 4 downregulated hub genes (FOXP3, CXCR4, MMP9, and CD69) were screened out for high degree. All these findings will help us to understand the potential molecular mechanisms of COVID-19, which is also of great significance for its diagnosis and prevention.
Highlights
Coronavirus disease 2019 (COVID-19) represents pneumonia created by a new type of coronavirus infection in 2019, which is a type of acutely infectious pneumonia [1]
Limma package in R was performed on the GSE151764 dataset, and 130 differentially expressed genes (DEGs) between 34 COVID-19-caused death lung tissue samples and 17 other disease-caused death lung tissue samples were comprehensively screened out, including 84 upregulated DEGs (P < 0.05, fold change (FC) > 2) and 46 downregulated DEGs (P < 0.05, FC < 0.5)
In the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, upregulated DEGs were significantly enriched in the AGE-RAGE signaling pathway in diabetic complications, coronavirus disease, amoebiasis, pertussis, ECM-receptor interaction, protein digestion and absorption, viral myocarditis, relaxin signaling pathway, human papillomavirus infection, and phagosome (Figure 2(b))
Summary
Coronavirus disease 2019 (COVID-19) represents pneumonia created by a new type of coronavirus infection in 2019, which is a type of acutely infectious pneumonia [1]. As a tool for genomics and genetics research, DNA microarrays are widely used to detect gene expression levels, identify gene sequences, and discover new genes and other related methods. Brandt et al detected mRNA expression levels of genes in pancreatic duct adenocarcinoma based on DNA microarray technology, which provides a direction for improving the poor prognosis and discovering new molecular markers and therapeutic targets [9]. Guo mentioned that the completion of human genome sequencing and the advancement of DNA microarray technology have accelerated the progress of genetic analysis on a genome-wide scale [10]. With the prevalence of microarray technology, a large number of data have been accessible, and the integration can conduct more in-depth research on molecular mechanisms. The protein-protein interaction (PPI) network of DEGs was designed for the hub genes’ identification. e results of the above studies will offer new clues for the COVID-19 treatment and reveal the relationship between COVID-19 and the lung
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
