Accumulating evidence suggests that endogenous retroviruses (ERVs) play an important role in the host response to infection and the development of disease. By analyzing ChIP-sequencing data sets, we show that SARS-CoV-2 infection induces H3K27 acetylation of several loci within the LTR69 subfamily of ERVs. Using functional assays, we identified one SARS-CoV-2-activated LTR69 locus, termed Dup69, which exhibits regulatory activity and is responsive to the transcription factors IRF3 and p65/RELA. LTR69_Dup69 is located about 500 bp upstream of a long non-coding RNA gene (ENSG00000289418) and within the PTPRN2 gene encoding a diabetes-associated autoantigen. Both ENSG00000289418 and PTPRN2 showed a significant increase in expression upon SARS-CoV-2 infection. Thus, our study sheds light on the interplay of exogenous with endogenous viruses and helps to understand how ERVs regulate gene expression during infection.
Keyphrases
- long non coding rna
- genome wide identification
- respiratory syndrome coronavirus
- poor prognosis
- transcription factor
- sars cov
- gene expression
- genome wide
- dna methylation
- copy number
- high throughput
- type diabetes
- coronavirus disease
- cardiovascular disease
- genome wide association study
- electronic health record
- single cell
- big data
- adipose tissue
- machine learning
- immune response
- circulating tumor cells
- artificial intelligence
- insulin resistance
- metabolic syndrome
- histone deacetylase