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10.4049/jimmunol.2001428

http://scihub22266oqcxt.onion/10.4049/jimmunol.2001428
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33782089!8183577!33782089
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suck abstract from ncbi


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pmid33782089      J+Immunol 2021 ; 206 (8): 1691-1696
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  • Cutting Edge: Reduced Adenosine-to-Inosine Editing of Endogenous Alu RNAs in Severe COVID-19 Disease #MMPMID33782089
  • Crooke PS 3rd; Tossberg JT; Porter KP; Aune TM
  • J Immunol 2021[Apr]; 206 (8): 1691-1696 PMID33782089show ga
  • Severe COVID-19 disease is associated with elevated inflammatory responses. One form of Aicardi-Goutieres syndrome caused by inactivating mutations in ADAR results in reduced adenosine-to-inosine (A-to-I) editing of endogenous dsRNAs, induction of IFNs, IFN-stimulated genes, other inflammatory mediators, morbidity, and mortality. Alu elements, approximately 10% of the human genome, are the most common A-to-I-editing sites. Using leukocyte whole-genome RNA-sequencing data, we found reduced A-to-I editing of Alu dsRNAs in patients with severe COVID-19 disease. Dendritic cells infected with COVID-19 also exhibit reduced A-to-I editing of Alu dsRNAs. Unedited Alu dsRNAs, but not edited Alu dsRNAs, are potent inducers of IRF and NF-kappaB transcriptional responses, IL6, IL8, and IFN-stimulated genes. Thus, decreased A-to-I editing that may lead to accumulation of unedited Alu dsRNAs and increased inflammatory responses is associated with severe COVID-19 disease.
  • |*SARS-CoV-2[MESH]
  • |*Severity of Illness Index[MESH]
  • |Adenosine/*genetics/metabolism[MESH]
  • |Alu Elements/*genetics[MESH]
  • |COVID-19/*genetics/pathology[MESH]
  • |Dendritic Cells/metabolism/virology[MESH]
  • |Genome, Human[MESH]
  • |Humans[MESH]
  • |Inosine/*genetics/metabolism[MESH]
  • |Interferon Regulatory Factors/metabolism[MESH]
  • |NF-kappa B/metabolism[MESH]
  • |RNA Editing/*genetics[MESH]
  • |RNA, Double-Stranded/*genetics[MESH]
  • |RNA-Seq[MESH]


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