Human T-cell leukaemia virus type 1: parasitism and pathogenesis.
Charles R M BanghamMasao MatsuokaPublished in: Philosophical transactions of the Royal Society of London. Series B, Biological sciences (2018)
Human T-cell leukaemia virus type 1 (HTLV-1) causes not only adult T-cell leukaemia-lymphoma (ATL), but also inflammatory diseases including HTLV-1-associated myelopathy/tropical spastic paraparesis. HTLV-1 transmits primarily through cell-to-cell contact, and generates abundant infected cells in the host in order to survive and transmit to a new host. The resulting high proviral load is closely associated with the development of ATL and inflammatory diseases. To increase the number of infected cells, HTLV-1 changes the immunophenotype of infected cells, induces proliferation and inhibits apoptosis through the cooperative actions of two viral genes, tax and HTLV-1 bZIP factor (HBZ). As a result, infected cells survive, proliferate and infiltrate into the tissues, which is critical for transmission of the virus. Thus, the strategy of this virus is indivisibly linked with its pathogenesis, providing a clue for prevention and treatment of HTLV-1-induced diseases.This article is part of the themed issue 'Human oncogenic viruses'.
Keyphrases
- cell cycle arrest
- induced apoptosis
- endothelial cells
- endoplasmic reticulum stress
- oxidative stress
- cell death
- pi k akt
- signaling pathway
- sars cov
- transcription factor
- spinal cord
- cell therapy
- induced pluripotent stem cells
- genome wide
- stem cells
- diffuse large b cell lymphoma
- cell proliferation
- mesenchymal stem cells
- spinal cord injury
- dna methylation
- drug induced
- stress induced