According to research published by Chinese scientists in the journal PLOS ONE, bioinformatics techniques have recently been used to unravel the genetic network and biological mechanisms behind coronavirus disease 2019 (COVID-19) myocarditis.

By examining the datasets of SARS-CoV-2-infected cardiac stem cells and SARS-CoV-2-infected patients with myocarditis, the researchers discovered genes that are associated to myocarditis. They carried out Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis for the set of common genes.

850 genes with differential expression in all were found. 449 of these genes showed an upregulation, whereas 401 showed a downregulation. Six crucial genes, including cyclin-dependent kinase 1 (CDK1), kinesin family member 20A (KIF20A), PDZ binding kinase (PBK), kinesin family member 2C (KIF2C), cell division cycle 20 (CDC20), and ubiquitin-conjugating enzyme E2 C (UBE2C), were specifically identified as being related to COVID-19 myocarditis. These genes might be used as possible biomarkers to identify myocarditis due to COVID-19.

The study also shows that SARS-CoV-2 alters the cell cycle and ubiquitin-mediated protein hydrolysis, two biological processes that are known to raise the risk of myocarditis.

Ten COVID-19 myocarditis gene-targeted medications were chosen, including Etoposide, Methotrexate, Lucanthone, Troglitazone, Ciclopirox, STL264925, Thalidomide, Genistein, Dmnq, and Testosterone, that may have a therapeutic effect on COVID-19-related myocarditis based on statistical significance. Among these medicines, it has been discovered that Troglitazone, Methotrexate, and Etoposide have anti-SARS-CoV-2 actions, such as the suppression of infection-related hyperinflammation and the inhibition of viral replication (cytokine storm). (News-Medical, 28 June 2022)