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Human T-cell leukaemia virus type 1: parasitism and pathogenesis

Publisher

ROYAL SOC
DOI: 10.1098/rstb.2016.0272

Keywords

HTLV-1; Tax; HBZ

Categories

Funding

  1. Japan Agency for Medical Research and Development, AMED
  2. JSPS KAKENHI [JP16H05336]
  3. Mitsubishi Foundation
  4. Medical Research Council UK [K019090]
  5. JSPS
  6. Grants-in-Aid for Scientific Research [17K19610, 16H05336] Funding Source: KAKEN

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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'.

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