HTLV-1 bZIP factor: the key viral gene for pathogenesis.
Masao MatsuokaJean-Michel MesnardPublished in: Retrovirology (2020)
Human T cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia-lymphoma (ATL) and inflammatory diseases. The HTLV-1 bZIP factor (HBZ) gene is constantly expressed in HTLV-1 infected cells and ATL cells. HBZ protein suppresses transcription of the tax gene through blocking the LTR recruitment of not only ATF/CREB factors but also CBP/p300. HBZ promotes transcription of Foxp3, CCR4, and T-cell immunoreceptor with Ig and ITIM domains (TIGIT). Thus, HBZ is critical for the immunophenotype of infected cells and ATL cells. HBZ also functions in its RNA form. HBZ RNA suppresses apoptosis and promotes proliferation of T cells. Since HBZ RNA is not recognized by cytotoxic T cells, HTLV-1 has a clever strategy for avoiding immune detection. HBZ plays central roles in maintaining infected T cells in vivo and determining their immunophenotype.
Keyphrases
- induced apoptosis
- cell cycle arrest
- endoplasmic reticulum stress
- transcription factor
- signaling pathway
- oxidative stress
- acute myeloid leukemia
- endothelial cells
- genome wide
- copy number
- regulatory t cells
- pi k akt
- sars cov
- dna methylation
- dendritic cells
- immune response
- diffuse large b cell lymphoma
- quantum dots
- loop mediated isothermal amplification
- anti inflammatory