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Updated: Jul 2, 2025

High-Throughput Transcriptome Analysis for Investigating Host-Pathogen Interactions
Published on: March 5, 2022
Blood transcriptome analysis uncovered COVID-19-myocarditis crosstalk
Shuang Liang1, Ying-Ying Zheng1, Ying Pan1
1Pharmacy Department, Hebei Medical University Third Hospital, Shijiazhuang, 050000, China.
Insights
COVID-19-related myocarditis is a significant cause of mortality. Researchers identified TBKBP1 and ERGIC1 as key genes involved in this condition, offering potential new therapeutic targets.
Area of Science:
- Cardiology
- Virology
- Genomics
Background:
- COVID-19-related myocarditis is a growing concern contributing to mortality.
- Understanding the molecular mechanisms of this condition is crucial.
Purpose of the Study:
- To identify hub genes associated with COVID-19-related myocarditis.
- To explore potential therapeutic targets for the condition.
Main Methods:
- Integrated gene expression profile analysis of COVID-19 and myocarditis datasets.
- Systems-biology approaches including network analysis and pathway enrichment.
- Verification with independent datasets and immune infiltration analysis.
Main Results:
- TBKBP1 and ERGIC1 identified as hub genes for COVID-19-related myocarditis.
- Expression levels of TBKBP1 and ERGIC1 effectively distinguish patients from controls.
- Potential drug targets including tamibarotene, methotrexate, and theophylline were identified.
Conclusions:
- TBKBP1 and ERGIC1 are crucial in COVID-19-related myocarditis development and linked to antiviral immunity.
- This research aids in understanding molecular mechanisms and identifying new therapeutic targets.
Background:
The condition of COVID-19-related myocarditis has emerged as a prominent contributor to COVID-19 mortality. As the epidemic persists, its incidence continues to rise. Despite ongoing efforts, the elucidation of COVID-19-related myocarditis underlying molecular mechanisms still requires further investigation.
Methods:
Hub genes for COVID-19-related myocarditis were screened by integrating gene expression profile analysis via differential expression in COVID-19 (GSE196822) and myocarditis (GSE148153 and GSE147517). After verification with independent datasets (GSE211979, GSE167028, GSE178491 and GSE215865), the hub genes were studied using a range of systems-biology approaches, such as ceRNA, TF-mRNA networks and PPI networks, as well as gene ontology, pathway enrichment, immune infiltration analysis and drug target identification.
Results:
TBKBP1 and ERGIC1 were identified as COVID-19-related myocarditis hub genes via integrated bioinformatics analysis. In addition, receiver operating characteristic curves constructed based on the expression levels of TBKBP1 and ERGIC1 could effectively distinguish healthy control individuals from patients with COVID-19. Functional enrichment analysis suggested several enriched biological pathways related to inflammation and immune response. Immune cell changes correlated with TBKBP1 and ERGIC1 levels in patients with COVID-19 or patients with COVID-19 and myocarditis. Tamibarotene, methotrexate and theophylline were identified as a potential drug targeting TBKBP1 and ERGIC1.
Conclusion:
TBKBP1 and ERGIC1 were identified as crucial genes in the development of COVID-19-related myocarditis and have demonstrated a strong association with innate antiviral immunity. The present work may be helpful for further investigation of the molecular mechanisms and new therapeutic drug targets correlated with myocarditis in COVID-19.

