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Whole-blood RNA-seq of severe COVID-19 reveals neutrophil immunothrombosis and reduced adaptive immune and ribosomal programs
Muhammad Abrar Yousaf
Abstract:
Severe coronavirus disease 2019 (COVID-19) is characterized by systemic inflammation, vascular injury, and immune dysfunction, yet the coordinated transcriptional programs underlying these processes remain incompletely resolved. Here, we re-analyzed whole-blood RNA sequencing data from 44 patients with severe COVID-19 and 10 healthy donors to identify disease-associated molecular pathways. Principal component analysis separated the two groups, and differential expression analysis identified 3,975 genes, including 2,796 upregulated and 1,179 downregulated transcripts. Upregulated genes were enriched for antimicrobial defense, innate and antiviral immunity, neutrophil extracellular trap formation, complement and coagulation, cell adhesion, extracellular matrix interactions, and cell cycle activity. Downregulated genes were dominated by ribosomal and translational programs, major histocompatibility complex class II antigen presentation, lymphocyte migration, and T-cell receptor signaling. Protein-interaction analysis further connected hub genes involved in inflammation, extracellular-matrix remodeling, cell cycling, T-cell biology, and ribosomal function. Together, these findings define severe COVID-19 as a transcriptional state of neutrophil-centered inflammation and immunothrombosis coupled to weakened adaptive immune and biosynthetic programs, providing a systems-level view of the molecular disturbances associated with severe disease.
Keywords:
COVID-19, neutrophil, immunothrombosis, RNA differential expression analysis
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