Virus-induced transposable element expression up-regulation in human and mouse host cells.
Marissa G MacchiettoRyan A LangloisSteven S ShenPublished in: Life science alliance (2020)
Virus-host cell interactions initiate a host cell-defensive response during virus infection. How transposable elements in the host cell respond to viral stress at the molecular level remains largely unclear. By reanalyzing next generation sequencing data sets from dozens of virus infection studies from the Gene Expression Omnibus database, we found that genome-wide transposon expression up-regulation in host cells occurs near antiviral response genes and exists in all studies regardless of virus, species, and host cell tissue types. Some transposons were found to be up-regulated almost immediately upon infection and before increases in virus replication and significant increases in interferon β expression. These findings indicate that transposon up-regulation is a common phenomenon during virus infection in human and mouse and that early up-regulated transposons are part of the first wave response during virus infection.
Keyphrases
- gene expression
- single cell
- genome wide
- poor prognosis
- cell therapy
- induced apoptosis
- endothelial cells
- dna methylation
- sars cov
- emergency department
- binding protein
- stem cells
- transcription factor
- oxidative stress
- immune response
- dendritic cells
- long non coding rna
- copy number
- endoplasmic reticulum stress
- cell death
- mesenchymal stem cells
- big data
- single molecule
- data analysis
- adverse drug
- heat stress
- disease virus
- bioinformatics analysis
- case control