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Philos Trans R Soc Lond B Biol Sci. 2017 Oct 19;372(1732). pii: 20160272. doi: 10.1098/rstb.2016.0272.

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

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Division of Infectious Diseases, Faculty of Medicine, Imperial College London, London W2 1PG, UK
Department of Hematology, Rheumatology, and Infectious Diseases, Kumamoto University Faculty of Life Sciences, 1-1-1 Honjo, Kumamoto 860-8556, Japan
Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan.


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'.


HBZ; HTLV-1; Tax

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