Long Covid involves activation of proinflammatory and immune exhaustion pathways
a day ago
- #Chronic Inflammation
- #Immune Dysfunction
- #Long COVID
- Long COVID (LC) is characterized by chronic symptoms persisting after acute SARS-CoV-2 infection.
- Key hypotheses for LC pathogenesis include persistent virus, autoimmunity, immune dysfunction, and complement activation.
- Immunological studies show persistent immune activation and proinflammatory responses in LC patients for over 180 days post-infection.
- Upregulated pathways in LC include JAK-STAT, IL-6 signaling, complement activation, and T cell exhaustion.
- Transcriptomic and proteomic analyses reveal metabolic dysregulation and chronic inflammation in LC.
- Early proinflammatory responses during acute infection predict the development of LC.
- Validation cohort confirms persistent upregulation of IL-6 and JAK-STAT pathways in LC.
- Potential therapeutic targets identified include JAK-STAT and IL-6 pathways.
- LC is associated with reduced cytotoxic T cell signaling and increased immune exhaustion.
- Sex differences suggest greater inflammation in females with LC compared to males.