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  • Journal article
    Manivannan K, Rowan AG, Tanaka Y, Taylor GP, Bangham CRMet al., 2016,

    CADM1/TSLC1 Identifies HTLV-1-Infected Cells and Determines Their Susceptibility to CTL-Mediated Lysis.

    , PLoS Pathog, Vol: 12

    Human T cell lymphotropic virus-1 (HTLV-1) primarily infects CD4+ T cells, causing inflammatory disorders or a T cell malignancy in 5% to 10% of carriers. The cytotoxic T lymphocyte (CTL) response is a key factor that controls the viral load and thus the risk of disease. The ability to detect the viral protein Tax in primary cells has made it possible to estimate the rate at which Tax-expressing infected cells are eliminated by CTLs in persistently infected people. However, most HTLV-1-infected cells are Tax-at a given time, and their immunophenotype is poorly defined. Here, we aimed to identify a cell-surface molecule expressed by both Tax+ and Tax-HTLV-1-infected cells and use it to analyse the CTL response in fresh peripheral blood mononuclear cells. Cell adhesion molecule 1 (CADM1/TSLC1) was the best single marker of HTLV-1 infection, identifying HTLV-1-infected cells with greater sensitivity and specificity than CD25, CCR4 or ICAM-1. CADM1+CD4+ T cells carried a median of 65% of proviral copies in peripheral blood. In a cohort of 23 individuals, we quantified the rate of CTL-mediated killing of Tax+ and Tax-CADM1+ cells. We show that CADM1 expression is associated with enhanced susceptibility of infected cells to CTL lysis: despite the immunodominance of Tax in the CTL response, Tax+CADM1- cells were inefficiently lysed by CTLs. Upregulation of the CADM1 ligand CRTAM on CD8+ T cells correlated with efficient lysis of infected cells. Tax-CADM1+ cells were lysed at a very low rate by autologous CTLs, however, were efficiently killed when loaded with exogenous peptide antigen. High expression of CADM1 on most HTLV-1-infected cells in the face of enhanced CTL counterselection implies that CADM1 confers a strong benefit on the virus.
  • Journal article
    Bangham CRM, Araujo A, Yamano Y, Taylor GPet al., 2015,

    HTLV-1-associated myelopathy/tropical spastic paraparesis.

    , Nature Reviews Disease Primers, Vol: 1, ISSN: 2056-676X

    Human T-lymphotropic virus 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a progressive disease of the CNS that causes weakness or paralysis of the legs, lower back pain and urinary symptoms. HAM/TSP was first described in Jamaica in the nineteenth century, but the aetiology of the condition, infection with the retrovirus HTLV-1, was only identified in the 1980s. HAM/TSP causes chronic disability and, accordingly, imposes a substantial health burden in areas where HTLV-1 infection is endemic. Since the discovery of the cause of HAM/TSP, considerable advances have been made in the understanding of the virology, immunology, cell biology and pathology of HTLV-1 infection and its associated diseases. However, progress has been limited by the lack of accurate animal models of the disease. Moreover, the treatment of HAM/TSP remains highly unsatisfactory: antiretroviral drugs have little impact on the infection and, although potential disease-modifying therapies are widely used, their value is unproved. At present, clinical management is focused on symptomatic treatment and counselling. Here, we summarize current knowledge on the epidemiology, pathogenesis and treatment of HAM/TSP and identify areas in which further research is needed.
  • Journal article
    Bangham CRM, Araujo A, Yamano Y, Taylor GPet al., 2015,

    HTLV-1-associated myelopathy/tropical spastic paraparesis

    , NATURE REVIEWS DISEASE PRIMERS, Vol: 1, ISSN: 2056-676X
  • Journal article
    Cook LB, Melamed A, Niederer H, Valganon M, Laydon D, Foroni L, Taylor GP, Matsuoka M, Bangham CRMet al., 2014,

    The role of HTLV-1 clonality, proviral structure, and genomic integration site in adult T-cell leukemia/lymphoma

    , Blood, Vol: 123, Pages: 3925-3931, ISSN: 0006-4971

    Adult T-cell leukemia/lymphoma (ATL) occurs in ∼5% of human T-lymphotropic virus type 1 (HTLV-1)–infected individuals and is conventionally thought to be a monoclonal disease in which a single HTLV-1+ T-cell clone progressively outcompetes others and undergoes malignant transformation. Here, using a sensitive high-throughput method, we quantified clonality in 197 ATL cases, identified genomic characteristics of the proviral integration sites in malignant and nonmalignant clones, and investigated the proviral features (genomic structure and 5′ long terminal repeat methylation) that determine its capacity to express the HTLV-1 oncoprotein Tax. Of the dominant, presumed malignant clones, 91% contained a single provirus. The genomic characteristics of the integration sites in the ATL clones resembled those of the frequent low-abundance clones (present in both ATL cases and carriers) and not those of the intermediate-abundance clones observed in 24% of ATL cases, suggesting that oligoclonal proliferation per se does not cause malignant transformation. Gene ontology analysis revealed an association in 6% of cases between ATL and integration near host genes in 3 functional categories, including genes previously implicated in hematologic malignancies. In all cases of HTLV-1 infection, regardless of ATL, there was evidence of preferential survival of the provirus in vivo in acrocentric chromosomes (13, 14, 15, 21, and 22).
  • Journal article
    Melamed A, Laydon DJ, Gillet NA, Tanaka Y, Taylor GP, Bangham CRMet al., 2013,

    Genome-wide Determinants of Proviral Targeting, Clonal Abundance and Expression in Natural HTLV-1 Infection

    , PLOS PATHOGENS, Vol: 9, ISSN: 1553-7366
  • Journal article
    Tattermusch S, Skinner JA, Chaussabel D, Banchereau J, Berry MP, McNab FW, O'Garra A, Taylor GP, Bangham CRMet al., 2012,

    Systems Biology Approaches Reveal a Specific Interferon-Inducible Signature in HTLV-1 Associated Myelopathy

    , PLOS PATHOGENS, Vol: 8, ISSN: 1553-7366
  • Journal article
    Gillet NA, Malani N, Melamed A, Gormley N, Carter R, Bentley D, Berry C, Bushman FD, Taylor GP, Bangham CRMet al., 2011,

    The host genomic environment of the provirus determines the abundance of HTLV-1-infected T-cell clones

    , BLOOD, Vol: 117, Pages: 3113-3122, ISSN: 0006-4971
  • Journal article
    Kattan T, MacNamara A, Rowan AG, Nose H, Mosley AJ, Tanaka Y, Taylor GP, Asquith B, Bangham CRMet al., 2009,

    The Avidity and Lytic Efficiency of the CTL Response to HTLV-1

    , JOURNAL OF IMMUNOLOGY, Vol: 182, Pages: 5723-5729, ISSN: 0022-1767
  • Journal article
    Palmowski MJ, Parker M, Choudhuri K, Chiu C, Callan MFC, van der Merwe PA, Cerundolo V, Gould KGet al., 2009,

    A Single-Chain H-2D(b) Molecule Presenting an Influenza Virus Nucleoprotein Epitope Shows Enhanced Ability at Stimulating CD8(+) T Cell Responses In Vivo

    , JOURNAL OF IMMUNOLOGY, Vol: 182, Pages: 4565-4571, ISSN: 0022-1767
  • Journal article
    Toulza F, Heaps A, Tanaka Y, Taylor GP, Bangham CRMet al., 2008,

    High frequency of CD4(+)FoxP3(+) cells in HTLV-1 infection: inverse correlation with HTLV-1-specific CTL response

    , BLOOD, Vol: 111, Pages: 5047-5053, ISSN: 0006-4971

This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.

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