1. Severe COVID-19 and long COVID are associated with high expression of STING, cGAS and IFN-α.
- Author
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Queiroz MAF, Brito WRDS, Pereira KAS, Pereira LMS, Amoras EDSG, Lima SS, Santos EFD, Costa FPD, Sarges KML, Cantanhede MHD, Brito MTFM, Silva ALSD, Leite MM, Viana MNDSA, Rodrigues FBB, Silva RD, Viana GMR, Chaves TDSS, Veríssimo AOL, Carvalho MDS, Henriques DF, Silva CPD, Nunes JAL, Costa IB, Cayres-Vallinoto IMV, Brasil-Costa I, Quaresma JAS, Falcão LFM, Santos EJMD, and Vallinoto ACR
- Subjects
- Humans, Interferon-alpha, Interleukin-6, Nucleotidyltransferases genetics, Nucleotidyltransferases metabolism, Signal Transduction genetics, Tumor Necrosis Factor-alpha genetics, COVID-19, Post-Acute COVID-19 Syndrome
- Abstract
The cGAS-STING pathway appears to contribute to dysregulated inflammation during coronavirus disease 2019 (COVID-19); however, inflammatory factors related to long COVID are still being investigated. In the present study, we evaluated the association of cGAS and STING gene expression levels and plasma IFN-α, TNF-α and IL-6 levels with COVID-19 severity in acute infection and long COVID, based on analysis of blood samples from 148 individuals, 87 with acute COVID-19 and 61 in the post-COVID-19 period. Quantification of gene expression was performed by real-time PCR, and cytokine levels were quantified by ELISA and flow cytometry. In acute COVID-19, cGAS, STING, IFN-α, TNF-α, and IL-6 levels were higher in patients with severe disease than in those with nonsevere manifestations (p < 0.05). Long COVID was associated with elevated cGAS, STING and IFN-α levels (p < 0.05). Activation of the cGAS-STING pathway may contribute to an intense systemic inflammatory state in severe COVID-19 and, after infection resolution, induce an autoinflammatory disease in some tissues, resulting in long COVID., (© 2024. The Author(s).)
- Published
- 2024
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