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

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          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’.

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          Cancer etiology. Variation in cancer risk among tissues can be explained by the number of stem cell divisions.

          Cristian Tomasetti, Bert Vogelstein (2015)
          Some tissue types give rise to human cancers millions of times more often than other tissue types. Although this has been recognized for more than a century, it has never been explained. Here, we show that the lifetime risk of cancers of many different types is strongly correlated (0.81) with the total number of divisions of the normal self-renewing cells maintaining that tissue's homeostasis. These results suggest that only a third of the variation in cancer risk among tissues is attributable to environmental factors or inherited predispositions. The majority is due to "bad luck," that is, random mutations arising during DNA replication in normal, noncancerous stem cells. This is important not only for understanding the disease but also for designing strategies to limit the mortality it causes. Copyright © 2015, American Association for the Advancement of Science.
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            Human T-cell leukaemia virus type 1 (HTLV-1) infectivity and cellular transformation.

            Masao Matsuoka, Kuan-Teh Jeang (2007)
            It has been 30 years since a 'new' leukaemia termed adult T-cell leukaemia (ATL) was described in Japan, and more than 25 years since the isolation of the retrovirus, human T-cell leukaemia virus type 1 (HTLV-1), that causes this disease. We discuss HTLV-1 infectivity and how the HTLV-1 Tax oncoprotein initiates transformation by creating a cellular environment favouring aneuploidy and clastogenic DNA damage. We also explore the contribution of a newly discovered protein and RNA on the HTLV-1 minus strand, HTLV-1 basic leucine zipper factor (HBZ), to the maintenance of virus-induced leukaemia.
            Article 0 comments Cited 278 times – based on 0 reviews     Review now
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              Diagnostic criteria and classification of clinical subtypes of adult T-cell leukaemia-lymphoma. A report from the Lymphoma Study Group (1984-87).

              M. Shimoyama (1991)
              The following diagnostic criteria are proposed to classify four clinical subtypes of HTLV-1 associated adult T-cell leukaemia-lymphoma (ATL): (1) Smouldering type, 5% or more abnormal lymphocytes of T-cell nature in PB, normal lymphocyte level (less than 4 x 10(9)/l), no hypercalcaemia (corrected calcium level less than 2.74 mmol/l), lactate dehydrogenase (LDH) value of up to 1.5 x the normal upper limit, no lymphadenopathy, no involvement of liver, spleen, central nervous system (CNS), bone and gastrointestinal tract, and neither ascites nor pleural effusion. Skin and pulmonary lesion(s) may be present. In case of less than 5% abnormal T-lymphocytes in PB, at least one of histologically-proven skin and pulmonary lesions should be present. (2) Chronic type, absolute lymphocytosis (4 x 10(9)/l or more) with T-lymphocytosis more than 3.5 x 10(9)/l, LDH value up to twice the normal upper limit, no hypercalcaemia, no involvement of CNS, bone and gastrointestinal tract, and neither ascites nor pleural effusion. Lymphadenopathy and involvement of liver, spleen, skin, and lung may be present, and 5% or more abnormal T-lymphocytes are seen in PB in most cases . (3) Lymphoma type, no lymphocytosis, 1% or less abnormal T-lymphocytes, and histologically-proven lymphadenopathy with or without extranodal lesions. (4) Acute type, remaining ATL patients who have usually leukaemic manifestation and tumour lesions, but are not classified as any of the three other types. A total of 818 ATL patients with a mean age of 57 years, newly diagnosed from 1983 to 1987, were analysed by this criteria. There were 448 males and 370 females, and 253 were still alive with a median follow-up time of 13.3 months from diagnosis, while 565 were dead with a median survival time (MST) of 5.4 months. MST was 6.2 months for acute type, 10.2 months for lymphoma type, 24.3 months for chronic type, and not yet reached for smouldering type. Projected 2- and 4-year survival rates were 16.7% and 5.0% for acute type, 21.3% and 5.7% for lymphoma type, 52.4% and 26.9% for chronic type, 77.7% and 62.8% for smouldering type, respectively. Distinct clinical features and laboratory findings of each clinical subtype are described.
              Article 0 comments Cited 242 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Philos Trans R Soc Lond B Biol Sci
                Journal ID (iso-abbrev): Philos. Trans. R. Soc. Lond., B, Biol. Sci
                Journal ID (publisher-id): RSTB
                Journal ID (hwp): royptb
                Title: Philosophical Transactions of the Royal Society B: Biological Sciences
                Publisher: The Royal Society
                ISSN (Print): 0962-8436
                ISSN (Electronic): 1471-2970
                Publication date (Print): 19 October 2017
                Publication date (Electronic): 11 September 2017
                Publication date PMC-release: 11 September 2017
                Volume: 372
                Issue: 1732 , Theme issue ‘Human oncogenic viruses’ compiled and edited by Yuan Chang, Patrick S. Moore and Robin A. Weiss
                Electronic Location Identifier: 20160272
                Affiliations
                [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
                Author notes

                One contribution of 14 to a theme issue ‘ Human oncogenic viruses’.

                Author information
                http://orcid.org/0000-0003-2624-3599
                http://orcid.org/0000-0002-0473-754X
                Article
                Publisher ID: rstb20160272
                DOI: 10.1098/rstb.2016.0272
                PMC ID: 5597739
                PubMed ID: 28893939
                SO-VID: 3033d90d-e87b-48bf-b64a-2d011652b823
                Copyright © © 2017 The Authors.
                License:

                Published by the Royal Society under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/4.0/, which permits unrestricted use, provided the original author and source are credited.

                History
                Date accepted : 9 June 2017
                Funding
                Funded by: Wellcome Trust, http://dx.doi.org/10.13039/100004440;
                Award ID: 100291
                Funded by: Japan Society for the Promotion of Science, http://dx.doi.org/10.13039/501100001691;
                Award ID: JP16H05336
                Funded by: Medical Research Council, http://dx.doi.org/10.13039/501100000265;
                Award ID: K019090
                Categories
                Subject: 1001
                Subject: 200
                Subject: Articles
                Subject: Review Article
                Custom metadata
                cover-date October 19, 2017

                ScienceOpen disciplines: Philosophy of science
                Keywords: htlv-1,tax,hbz
                Data availability:
                ScienceOpen disciplines: Philosophy of science
                Keywords: htlv-1, tax, hbz

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