Abstract
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’.
Highlights
Human T-cell leukaemia virus type 1 (HTLV-1) has a long history in the human, after interspecies transmission from monkeys
We show how HTLV-1 transmits and survives in vivo, and how the strategy of the virus is associated with the pathogenesis of malignant and inflammatory diseases, with a special focus on adult T-cell leukaemia-lymphoma (ATL)
Recent evidence from high-throughput sequencing and quantification of HTLV-1 integration sites has changed this view: the number of HTLV-1-positive T-cell clones in the circulation in each host is of the order of 104–105 [31], and it is the clonal diversity, not the degree of oligoclonal proliferation, that correlates with the proviral load [37]
Summary
Human T-cell leukaemia virus type 1 (HTLV-1) has a long history in the human, after interspecies transmission from monkeys. HTLV-1 has a simian origin called simian T-cell leukaemia virus type 1 (STLV-1). STLV-1 is endemic in many species of Old-World monkeys and apes. The precise origins of the ancestors of HTLV-1 present in humans remain uncertain, i.e. the species of monkey and the time and place of the putative interspecies transmission. Interspecies transmission from monkeys and apes infected by STLV-1 strains are continuing, at least in Central Africa, as reported in [2]. We show how HTLV-1 transmits and survives in vivo, and how the strategy of the virus is associated with the pathogenesis of malignant and inflammatory diseases, with a special focus on adult T-cell leukaemia-lymphoma (ATL)
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