Transcriptomic profiling of disease severity in patients with COVID-19 reveals role of blood clotting and vasculature related genes

COVID-19 caused by SARS-CoV-2 manifests as a range of symptoms. Understanding the molecular mechanisms responsible for immuno-pathogenesis of disease is important for treatment and management of COVID-19. We examined host transcriptomes in moderate and severe COVID-19 cases with a view to identifying pathways that affect its progression. RNA extracted from whole blood of COVID-19 cases was analysed by microarray analysis. Moderate and severe cases were compared with healthy controls and differentially regulated genes (DEGs) categorized into cellular pathways.

DEGs in COVID-19 cases were mostly related to host immune activation and cytokine signaling, pathogen uptake, host defenses, blood and vasculature genes, and SARS-CoV-2- and other virus-affected pathways. The DEGs in these pathways were increased in severe compared with moderate cases. In a severe COVID-19 patient with an unfavourable outcome we observed dysregulation of genes in platelet homeostasis and cardiac conduction and fibrin clotting with disease progression.

COVID-19 morbidity is associated with cytokine activation, cardiovascular risk and thrombosis. We identified DEGs related to dysregulation of blood clotting and homeostasis, platelet activation pathways and to be associated with disease progression. These can be biomarkers of disease progression and also potential targets for treatment interventions in COVID-19.