Preprint Persistent Activation of Chronic Inflammatory Pathways in Long Covid, 2024, Aid et al.

Persistent Activation of Chronic Inflammatory Pathways in Long Covid
Malika Aid; Katherine McMahan; Nicole Hachmann; Jessica Miller; Erica Borducchi; David Hope; Marjorie Rowe; Eleanor Schonberg; Siline Thai; Ai-ris Collier; Janet Mullington; Dan Barouch

Long Covid, or Post-Acute Sequelae of COVID-19 (PASC), involves a spectrum of chronic symptoms following resolution of acute SARS-CoV-2 infection. Current hypotheses for the pathogenesis of Long Covid include persistent SARS-CoV-2, activation of other viruses, tissue damage, autoimmunity, endocrine insufficiency, immune dysfunction, and complement activation.

We evaluated 142 participants, including uninfected controls (N=35), acutely infected individuals (N=54), convalescent controls (N=25), and Long Covid patients (N=28), by comprehensive immunologic, virologic, transcriptomic, and proteomic analyses.

Long Covid was characterized by persistent inflammatory pathways compared with convalescent controls and uninfected controls, including upregulation of IL-6 and JAK-STAT pathways as well as activation of coagulation, complement, metabolism, and T cell exhaustion pathways. Moreover, robust activation of these pathways during acute COVID-19 infection correlated with the subsequent development of Long Covid. In an independent validation cohort (N=47), Long Covid patients had higher levels of plasma IL-6R compared with convalescent controls and uninfected controls.

These data demonstrate that Long Covid is characterized by persistent activation of chronic inflammatory pathways, suggesting novel therapeutic targets and biomarkers of disease.


Link | PDF (Preprint: BioRxiv) [Open Access]

 

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Thanks for that—it does look interesting.