Immunothrombosis in hospitalized COVID-19 patients identified by multiomics profiling and linked to postacute complications
🚨INTERESTING New Latvian/Swedish multi-omics study shows immunothrombosis never fully switched off in longC0VID patients: 3 months after COVID hospitalization, your blood is still biologically “clot-ready.”
➡️What makes this study so important:
1. It reinforces that immunothrombosis (the interplay of complement, NETs, and platelets) is a central driver in severe acute COVID-19 and can persist in longC0VID,
2. It confirms persistent endothelial Dysfunction/Endotheliopathy in longC0VID patients, consistent with earlier studies on vascular damage and microclots,
3. It aligns with prior evidence of mitochondrial dysfunction during the acute phase, followed by partial repair mechanisms,
4. The persistent complement activation they observed fits with other recent multi-omics studies showing ongoing complement dysregulation in longC0VID.
➡️Study:
1. Prospective longitudinal multi-omics study of 81 hospitalized COVID-19 patients tracked whole-blood transcriptomics, urine metabolomics (46 analytes), and 13 kidney-injury biomarkers at acute admission, ~1 month, and ~3 months post-hospitalization,
2. Patients stratified by EHR into recovered (n=35) versus long COVID (n=46) groups based on a PASC diagnoses within 12 months,
3. None of the 81 hospitalized patients were vaccinated,
4. Acute phase dominated by interconnected immunothrombosis: strong upregulation of complement (C1QA/B/C), NETosis (PADI4, MPO), and platelet-activation genes (ITGA2B, ITGB3), plus mitochondrial dysfunction (HIF1A/EPAS1 up, OXPHOS down, Warburg-like glycolysis) and elevated renal injury markers (KIM-1 etc.),
5. Most immune, mitochondrial, and metabolomic changes largely normalized by 1–3 months, with rebound in mitophagy/heme genes (PINK1, OPA1, FECH) indicating repair,
6. At 3 months, longC0VID patients showed a distinct transcriptional signature of persistent endothelial activation (↑VWF, PROS1, ITGA2B/ITGB3), complement dysregulation (CFH), and low-grade vascular inflammation/platelet reactivity (CXCL5, ALOX12) that was absent in recovered individuals,
7. No significant late differences in urine metabolomics or kidney biomarkers between groups.
➡️They conclude with their Highlight-points:
• Severe COVID-19 induces immunothrombosis-associated molecular programs,
• Acute COVID-19 is associated with mitochondrial metabolic dysregulation,
• Urine profiling indicates gradual renal recovery after hospitalization,
• LongC0VID patients retain endothelial-associated activation signatures.
‼️So, even after apparent clinical recovery, immunothrombosis leaves a persistent molecular scar of endothelial activation and prothrombotic signalling in longC0VID patients at three months, revealing that the acute vascular battlefield never fully quiets in those who remain symptomatic.
→Three months post Covid-19, longC0VID patient’s blood is still biologically primed to clot!
#AvoidSars2 #AvoidReinfections
cell.com/iscience/fulltext/S…