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Time-Series Bioinformatics Analysis of Sars-Cov-Infected Cells to Identify the Biological Processes Associated With Severe Acute Respiratory Syndrome Publisher Pubmed



Fatehi R1 ; Khosravian F2, 3 ; Salehi M2, 3 ; Kazemi M1, 4
Authors
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Authors Affiliations
  1. 1. Department of Genetics and Molecular Biology, Isfahan University of Medical Sciences, Isfahan, Iran
  2. 2. Cellular, Molecular and Genetics Research Center, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3. Medical Genetics Research Center of Genome, Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Reproductive Sciences and Sexual Health Research Center, Isfahan University of Medical Science, Isfahan, Iran

Source: Human Antibodies Published:2024


Abstract

BACKGROUND: The COVID-19 pandemic, caused by the new virus of the coronavirus family, SARS-CoV-2, could lead to acute respiratory syndrome. The molecular mechanisms related to this disorder are still debatable. METHODS: In this study to understand the pathogenicity mechanism of SARS-CoV-2, using the bioinformatics approaches, we investigated the expression of involved genes, their regulatory, and main signaling pathways during the time on days 1, 2, 3, and 4 of SARS-CoV infected cells. RESULTS: Here, our investigation shows the complex changes in gene expression on days 2 and 3 post-infection. The functional analysis showed that especially related to immune response, response to other organisms, and defense response. IL6-AS1 is the predicted long non-coding RNA and is a key regulator during infection. In this study, for the first time has been reported the role of IL6-AS1. Also, the correlation of differential expression genes with the level of immune infiltration was shown in the relationship of Natural killer cells and T cell CD 4+ with DE genes. CONCLUSION: In the current study, identification of the altered expression pattern of genes in SARS-CoV-infected cells in time course also can help identify and link the molecular mechanisms and explore the holistic view of infection of SARS-CoV-2. © 2024 IOS Press. All rights reserved.
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