Cutting Edge: Reduced Adenosine-to-Inosine Editing of Endogenous Alu RNAs in Severe COVID-19 Disease.
J Immunol
; 206(8): 1691-1696, 2021 04 15.
Article
in English
| MEDLINE | ID: covidwho-1158408
ABSTRACT
Severe COVID-19 disease is associated with elevated inflammatory responses. One form of Aicardi-Goutières 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, â¼10% 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-κB 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.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Severity of Illness Index
/
RNA, Double-Stranded
/
Adenosine
/
RNA Editing
/
Alu Elements
/
SARS-CoV-2
/
COVID-19
/
Inosine
Type of study:
Prognostic study
Limits:
Humans
Language:
English
Journal:
J Immunol
Year:
2021
Document Type:
Article
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