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Updated: Jun 27, 2025
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High-Throughput Transcriptome Analysis for Investigating Host-Pathogen Interactions
Published on: March 5, 2022
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CompCorona: A web application for comparative transcriptome analyses of coronaviruses reveals SARS-CoV-2-specific
Rana Salihoğlu1,2, Fatih Saraçoğlu3, Mustafa Sibai4
1Department of Bioinformatics, University of Würzburg, Würzburg, Germany.
Turkish Journal of Biology = Turk Biyoloji Dergisi
|April 29, 2024
Summary
SARS-CoV-2 infection uniquely downregulates key genes in lung cells, potentially causing epithelial dysfunction. Our new tool, CompCorona, aids research into coronavirus disease mechanisms and long COVID.
Area of Science:
- Virology and transcriptomics
- Immunology and host-pathogen interactions
- Computational biology and bioinformatics
Background:
- Understanding host transcriptomic responses to SARS-CoV-2 is vital for addressing long COVID and related inflammatory conditions.
- Investigating shared and distinct mechanisms across Coronaviridae family infections is crucial for disease progression insights.
Purpose of the Study:
- To analyze and compare host transcriptomic responses to SARS-CoV-2, SARS-CoV, and MERS-CoV infections.
- To develop an interactive tool (CompCorona) for visualizing and analyzing viral transcriptomic data.
- To identify specific host response patterns associated with SARS-CoV-2 infection.
Main Methods:
- Comprehensive transcriptome and enrichment analyses of lung and peripheral blood mononuclear cells (PBMCs) infected with SARS-CoV-2, SARS-CoV, and MERS-CoV.
- Development and utilization of CompCorona, an online tool for 2D/3D principal component analysis (PCA) and pathway analysis.
- Public release of preprocessed datasets for comparative analysis.
Main Results:
- SARS-CoV-2 infection uniquely downregulates angiogenin (ANG) and vascular endothelial growth factor A (VEGFA) in lung cells, indicating potential epithelial and vascular dysfunction.
- Suppression of TNF signaling and activation of complement/coagulation pathways observed in SARS-CoV-2 infected cells.
- Ribosome pathway suppression was a common finding across all three tested coronaviruses.
Conclusions:
- SARS-CoV-2 infection may induce pulmonary epithelial dysfunction distinct from other CoVs.
- The CompCorona tool and associated datasets offer a valuable resource for researching CoV-associated syndromes and long COVID.
- Comparative transcriptomic analysis reveals specific host responses to SARS-CoV-2 infection.
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