COVID-19 activates endogenous retroviruses within our genome Coronavirus Disease COVID SARSCoV2 endogenous retroviruses virology biorxivpreprint Cornell DZNE_en uni_tue DBT_inStem
By Bhavana KunkalikarMar 28 2023Reviewed by Benedette Cuffari, M.Sc. *Important notice: bioRxiv publishes preliminary scientific reports that are not peer-reviewed and, therefore, should not be regarded as conclusive, guide clinical practice/health-related behavior, or treated as established information.
Study: SARS-CoV-2 infection activates endogenous retroviruses of the LTR69 subfamily. Image Credit: Numstocker / Shutterstock.com To examine the enhancer activity of long terminal repeat -103 and LTR69 in the absence and presence of SARS-CoV-2, the team analyzed publicly available ChIP-seq data associated with Histone H3 Lysine 27 acetylation in A549-angiotensin-converting enzyme 2 cells. To determine whether any of the SARS-CoV-2-activated LTR69 repeats elicit regulatory influences, their potential enhancer activities were examined. Five representative candidates were inserted into enhancer reporter vectors.
Omics eBook Compilation of the top interviews, articles, and news in the last year. Download a free copy The transcription start site profile plot over LTR69 loci revealed enrichment of H3K27Ac marks in infected cells as compared to uninfected cells. No considerable enrichment of enhancer marks was observed on the LTR103_Mam loci.
Dup69 resides in an intron of protein tyrosine phosphatase receptor type N2 , which is approximately 500 nucleotides upstream of a long non-coding RNA gene called ENSG00000289418, according to an examination of the respective gene locus. PTPRN2 encodes a tyrosine phosphatase receptor that is a significant autoantigen in type 1 diabetes.
Several probable binding sites for nuclear factor kappa B subunits, signal transducer and activator of transcription 1 , and IRF3 were identified. Furthermore, p65/RelA and an active mutant of IRF3, but not STAT1, may augment the LTR69-mediated increase in reporter gene expression. Consistent with the activation of IRF3 and NF-κB upon innate sensing, synthetic double-stranded RNA analog polyI:C dramatically boosted LTR69_Dup69 activity.
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