Adult T cell leukemia: A tale of two T cells

Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, Virginia 23501, USA.
Journal of Clinical Investigation (Impact Factor: 13.22). 05/2006; 116(4):858-60. DOI: 10.1172/JCI28140
Source: PubMed


Human T cell leukemia virus type 1 (HTLV-1) is the etiologic agent for the development of an aggressive hematologic neoplasia termed adult T cell leukemia/lymphoma (ATLL). Although the virus infects T cell subsets that display either CD4 or CD8 cell surface markers, the leukemic cell is exclusively of the CD4+ subtype. In the article by Sibon et al. in this issue of the JCI, the authors demonstrate that the molecular basis for clonal expansion differs between these 2 infected T cell populations (see the related article beginning on page 974). The molecular events associated with a preleukemic state, such as genomic instability, polynucleation, and cell cycle redistribution, were only observed in CD4+ T cells. This finding provides a molecular-based mechanism for the restriction of the leukemic phenotype to the CD4+ T cell subtype.

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Available from: Oliver John Semmes, Mar 18, 2014
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    • "While infection with this virus can lead to several disorders [2], it most notably leads to adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). ATL is an aggressive hematopoietic disease affecting approximately 3% of HTLV-1 infected individuals [3]. Currently there are no diagnostic tools available for early detection or disease state assessment associated with ATL induced by HTLV-1 infection. "
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    • "Although several studies showed the high prevalence of HTLV-I in Japan southwest, however the prevalence of virus in adjacent countries like Korea, China, Eastern Russia and Khorasan in Iran is low.[1] HTLV-I can induce several diseases such as Adult T Cell Leukemia (ATL), Human T Lymphotropic Virus type I Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP), sensori-motor polyneuropathy and optic neuritis.[2][3][4] Many cases of disease due to transmission are well established and the disease is known as a sexual transmitted disease.[5] "
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    ABSTRACT: Because of the low prevalence of Human T Lymphotropic Virus type I (HTLV-I) in comparison with Khorasan Province, considering HTLV-I as an etiology of spastic paraparesia, it may be neglected in evaluation of spastic paraparesis in the other regions of Iran. Some reports of spastic paraparetic patients due to HTLV-I infection in West Azarbaijan, caused us to reconsider the importance of HTLV-I epidemiology in the other areas of the country. All spastic paraparetic patients who referred to Motahari and Imam Khomeini educational hospitals of Urmia from September 2004 to September 2007 were assessed for HTLV-I infection antibodies. In our 3 years study, 11 cases were diagnosed as Human T Lymphotropic Virus type I Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP, 2 males and 9 females).The mean age of patients at the time of diagnosis was 45.8 years. Dorsal and cervical MRI of all patients was normal. Serum Enzyme-Linked Immuno-Sorbent Assay (ELISA) and Western blot (WB) for anti HTLV-I antibody in all patients was positive. Four patients underwent for lumbar puncture in which were normal in respect of cells and biochemistry, but positive for anti-HLTLV-I antibodies. HAM/TSP detection in West Azarbaijan in spite of its long distance from Khorasan Province shows the importance of anti-HTLV-I Ab assay in the blood and CSF of every spastic paraparetic patient all over the country.
    06/2011; 13(6):428-30.
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    ABSTRACT: The human T-cell leukemia virus type 1 (HTLV-I) causes adult T-cell leukemia and several severe chronic diseases. HTLV-I protease (PR) inhibition stops the propagation of the virus. Herein, truncation studies were performed on potent octapeptidie HTLV-I PR inhibitor KNI-10161 to derive small hexapeptide KNI-10127 with some loss in activity. After performing residue-substitution studies on compound KNI-10127, HTLV-I PR inhibitory activity was recovered in inhibitor KNI-10166. (c) 2007 Elsevier Ltd. All rights reserved.
    Bioorganic & Medicinal Chemistry Letters 07/2007; 17(12):3276-80. DOI:10.1016/j.bmcl.2007.04.019 · 2.42 Impact Factor
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