Cell type specificity of human T cell leukemia virus 1 has been proposed as a possible reason for differential viral outcome in primary target cells versus secondary. Through chromatin remodeling, the HTLV-1 transactivator protein Tax interacts with cellular factors at the chromosomally integrated viral promoter to activate downstream genes and control viral transcription. RNA interference is the host innate defense mechanism mediated by short RNA species (siRNA or miRNA) that regulate gene expression. There exists a close collaborative functioning of cellular transcription factors with miRNA in order to regulate the expression of a number of eukaryotic genes including those involved in suppression of cell growth, induction of apoptosis, as well as repressing viral replication and propagation. In addition, it has been suggested that retroviral latency is influenced by chromatin alterations brought about by miRNA. Since Tax requires the assembly of transcriptional cofactors to carry out viral gene expression, there might be a close association between miRNA influencing chromatin alterations and Tax-mediated LTR activation. Herein we explore the possible interplay between HTLV-1 infection and miRNA pathways resulting in chromatin reorganization as one of the mechanisms determining HTLV-1 cell specificity and viral fate in different cell types.
Keyphrases
- gene expression
- transcription factor
- sars cov
- genome wide
- dna methylation
- dna damage
- cell cycle arrest
- genome wide identification
- oxidative stress
- induced apoptosis
- single cell
- immune response
- binding protein
- endothelial cells
- acute myeloid leukemia
- dna binding
- poor prognosis
- endoplasmic reticulum stress
- signaling pathway
- cell proliferation
- heat shock
- quality improvement
- nucleic acid
- induced pluripotent stem cells
- amino acid
- genetic diversity