Nawal Helmi, Dalia Alammari and Mohammad Mobashir*
Background: Coronavirus is an enveloped positive-sense RNA virus and is characterized by club-like spikes projecting from its surface which is commonly associated with acute respiratory infections in humans but its ability to infect multiple host species and multiple diseases brings it to a complex pathogen group. The frequent interactions of wild animals with humans it is more prevalent a common source of such infections and SARS—CoV and MERS—CoV are the zoonotic pathogens among the leading cause of severe respiratory diseases in humans.
Aim: The major purpose of this study was to study the gene expression profiling for those human samples which are infected with coronavirus or uninfected and compare the differential expression patterns and its functional impact.
Methods: For this purpose, the previously studied samples have been collected from public database and the study had been performed and it includes gene expression analysis, pathway analysis, and the network-level understanding. The analysis presents the data for the differentially expressed genes, enriched pathways and the networks for the potential genes and gene sets. In terms of gene expression and the linkage of COVID-19 with type-2 diabetes.
Results: We observe that there are a large number of genes which show altered gene expression pattern than the normal for coronavirus infection while in terms of pathways it appears that there are few sets of functions which are affected due to altered gene expression and they infer to infection, inflammation, and the immune system.
Conclusions: Based on our study, we conclude that the potential genes which are affected due to infection are NFKBIA, MYC, FOXO3, BIRC3, ICAM1, IL8, CXCL1/2/5, GADD45A, RELB, SGK1, AREG, BBC3, DDIT3/4, EGR1, MTHFD2, and SESN2 and the functional changes are mainly associated with these pathways TNF, cytokine, NF—kB, TLR, TCR, BCR, Foxo, and TGF signaling pathways are among them and there are additional pathways such as hippo signaling, apoptosis, estrogen signaling, regulating pluropotency of stem cells, ErbB, Wnt, p53, cAMP, MAPK, PI3K—AKT, oxidative phosphorylation, protein processing in endoplasmic reticulum, prolactin signaling, adipocytokine, neurotrophine signaling, and longevity regulating pathways. SMARCD3, PARL, GLIPR1, STAT2, PMAIP1, GP1BA, and TOX genes and PI3K-Akt, focal adhesion, Foxo, phagosome, adrenergic, osteoclast differentiation, platelet activation, insulin, cytokine-cytokine interaction, apoptosis, ECM, JAK-STAT, and oxytocine signaling appear as the linkage between COVID-19 and Type-2 diabetes.
Coronavirus, gene expression profiling, pathological biomarkers, infection and immune system, differentially expressed genes, enriched pathways, networks.
Department of Biochemistry, College of Sciences, University of Jeddah, Jeddah, Department of Microbiology and Immunology, Faculty of Medicine, Ibn Sina National College, Jeddah, Department of Microbiology, Tumor and Cell Biology (MTC) Karolinska Institute, Novels väg 16, 17165 Solna Stockholm