Journal
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES
Volume 372, Issue 1732, Pages -Publisher
ROYAL SOC
DOI: 10.1098/rstb.2016.0272
Keywords
HTLV-1; Tax; HBZ
Categories
Funding
- Japan Agency for Medical Research and Development, AMED
- JSPS KAKENHI [JP16H05336]
- Mitsubishi Foundation
- Medical Research Council UK [K019090]
- JSPS
- Grants-in-Aid for Scientific Research [17K19610, 16H05336] Funding Source: KAKEN
Ask authors/readers for more resources
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'.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available