The immunopathology of post-acute sequelae of SARS-CoV-2 infection: highlighting the knowledge gaps eLife postcovid longcovid longCOVID PASC COVID COVID19 SARSCoV2 immunopathology
By Neha MathurMay 31 2023Reviewed by Lily Ramsey, LLM In a recent article published in eLife, researchers highlighted the knowledge gaps in the immunopathology of post-acute sequelae of severe acute respiratory syndrome coronavirus 2 infection , or long COVID and acute coronavirus disease 2019 .
Background Understanding the mechanisms underlying PASC is crucial for the development of appropriate precision therapies which could help restore healthy immune function in PASC patients. Though not released simultaneously, both granulocyte-macrophage colony-stimulating factor and cytokines are involved in the immune response to SARS-CoV-2 and possibly play a role in COVID-19 severity.
Innate and adaptive immunity in COVID-19 and PASC: role of neutrophils, macrophages, mast cells, and autoantibodies Excessive neutrophil activation is an important predictor of whether the disease trajectory would take a more severe course. Researchers Kaiser et al. and Vanderbeke et al. have implicated the amplification of inflammatory and pro-thrombotic loops via interactions with other immune cells resulting in cytokine storms that govern neutrophil activation.
A dysregulated monocyte/macrophage inflammatory response to SARS-CoV-2 possibly contributes to disease severity and mortality in COVID-19 patients. However, data on aberrant activation of monocytes and macrophages in PASC is scarce. A few studies also investigated longitudinal changes in T cell profiles and T cell dynamics in patients with PASC.
Thus, children with MIS-C have lower SARS-CoV-2-specific CD4+ and CD8+ T cell responses to SARS-CoV-2 antigens, e.g., spike protein. Cheng et al. observed a shift toward TRBV genes in adults with severe acute COVID-19, but information on TCR repertoire shifts in adult patients with long COVID is scarce.
In a second scenario, IgG autoantibodies are produced de novo during infection, indicating that severe COVID-19 can break tolerance to self. Accordingly, Woodruff et al. found enrichment of extrafollicular B cells in subjects with severe and fatal COVID-19.
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