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

Author:

Bangham Charles R. M.1ORCID,Matsuoka Masao23ORCID

Affiliation:

1. Division of Infectious Diseases, Faculty of Medicine, Imperial College London, London W2 1PG, UK

2. Department of Hematology, Rheumatology, and Infectious Diseases, Kumamoto University Faculty of Life Sciences, 1-1-1 Honjo, Kumamoto 860-8556, Japan

3. Institute for Frontier Life and Medical Sciences, Kyoto University, 53 Shogoin Kawahara-cho, Sakyo-ku, Kyoto 606-8507, Japan

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’.

Funder

Wellcome Trust

Japan Society for the Promotion of Science

Medical Research Council

Publisher

The Royal Society

Subject

General Agricultural and Biological Sciences,General Biochemistry, Genetics and Molecular Biology

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