Publications
303 results found
Melamed A, Laydon DJ, Gillet NA, et al., 2013, Genome-wide Determinants of Proviral Targeting, Clonal Abundance and Expression in Natural HTLV-1 Infection, PLOS PATHOGENS, Vol: 9, ISSN: 1553-7366
- Author Web Link
- Open Access Link
- Cite
- Citations: 76
Chataway J, Schuerer N, Alsanousi A, et al., 2013, THE MS-STAT TRIAL: High Dose Simvastatin Slows Brain Atrophy and Delays Disability in Secondary Progressive Multiple Sclerosis: A Phase II Placebo-Controlled Trial, 65th Annual Meeting of the American-Academy-of-Neurology (AAN), Publisher: LIPPINCOTT WILLIAMS & WILKINS, ISSN: 0028-3878
- Author Web Link
- Cite
- Citations: 4
Cook LB, Rowan AG, Melamed A, et al., 2012, HTLV-1-infected T cells contain a single integrated provirus in natural infection, BLOOD, Vol: 120, Pages: 3488-3490, ISSN: 0006-4971
- Author Web Link
- Cite
- Citations: 79
Tattermusch S, Bangham CRM, 2012, HTLV-1 infection: what determines the risk of inflammatory disease?, TRENDS IN MICROBIOLOGY, Vol: 20, Pages: 494-500, ISSN: 0966-842X
- Author Web Link
- Cite
- Citations: 16
Martin F, Castro H, Gabriel C, et al., 2012, Ciclosporin A Proof of Concept Study in Patients with Active, Progressive HTLV-1 Associated Myelopathy/Tropical Spastic Paraparesis, PLOS NEGLECTED TROPICAL DISEASES, Vol: 6, ISSN: 1935-2735
- Author Web Link
- Open Access Link
- Cite
- Citations: 22
Berry CC, Gillet NA, Melamed A, et al., 2012, Estimating abundances of retroviral insertion sites from DNA fragment length data, BIOINFORMATICS, Vol: 28, Pages: 755-762, ISSN: 1367-4803
- Author Web Link
- Cite
- Citations: 91
Tattermusch S, Skinner JA, Chaussabel D, et al., 2012, Systems Biology Approaches Reveal a Specific Interferon-Inducible Signature in HTLV-1 Associated Myelopathy, PLOS PATHOGENS, Vol: 8, ISSN: 1553-7366
- Author Web Link
- Open Access Link
- Cite
- Citations: 71
Saito M, Bangham CRM, 2012, Immunopathogenesis of human T-cell leukemia virus type-1-associated myelopathy/tropical spastic paraparesis: recent perspectives., Leuk Res Treatment, Vol: 2012
Human T-cell leukemia virus type-1 (HTLV-1) is a replication-competent human retrovirus associated with two distinct types of disease only in a minority of infected individuals: the malignancy known as adult T-cell leukemia (ATL) and a chronic inflammatory central nervous system disease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). HAM/TSP is a chronic progressive myelopathy characterized by spastic paraparesis, sphincter dysfunction, and mild sensory disturbance in the lower extremities. Although the factors that cause these different manifestations of HTLV-1 infection are not fully understood, accumulating evidence from host population genetics, viral genetics, DNA expression microarrays, and assays of lymphocyte function suggests that complex virus-host interactions and the host immune response play an important role in the pathogenesis of HAM/TSP. Especially, the efficiency of an individual's cytotoxic T-cell (CTL) response to HTLV-1 limits the HTLV-1 proviral load and the risk of HAM/TSP. This paper focuses on the recent advances in HAM/TSP research with the aim to identify the precise mechanisms of disease, in order to develop effective treatment and prevention.
Saito M, Jain P, Tsukasaki K, et al., 2012, HTLV-1 Infection and Its Associated Diseases., Leuk Res Treatment, Vol: 2012
Olindo S, Belrose G, Gillet N, et al., 2011, Safety of long-term treatment of HAM/TSP patients with valproic acid, BLOOD, Vol: 118, Pages: 6306-6309, ISSN: 0006-4971
- Author Web Link
- Cite
- Citations: 34
Rowan AG, Asquith B, Taylor GP, et al., 2011, Susceptibility of HBZ and Tax expressing primary HTLV-1+ T cell clones to CTL lysis, Retrovirology, Vol: 8
Hlela C, Gillet N, Bangham C, et al., 2011, Human T-lymphotropic virus type 1(HTLV-1) integration, HTLV-1-associated infective dermatitis (IDH) and the risk of Adult T cell leukaemia/lymphoma (ATLL), Retrovirology, Vol: 8
Hodson A, Demontis MA, Gillet N, et al., 2011, First line treatment of acute and chronic ATLL with zidovudine (AZT) and interferon alpha (IFN-α): haematological and molecular responses, Retrovirology, Vol: 8
Nejmeddine M, Clerc I, Taylor GP, et al., 2011, Exclusion of actin microfilaments from the cell-cell contact zone in HTLV-1 infected T-lymphocyte during the establishment of a functional virological synapse, Retrovirology, Vol: 8
Kirk P, Witkover A, Courtney A, et al., 2011, Three plasma biomarkers of HTLV-1-associated myelopathy/tropical spastic paraparesis, Retrovirology, Vol: 8
Rende F, Cavallari I, Corradin A, et al., 2011, Kinetics and intracellular compartmentalization of HTLV-1 gene expression, Retrovirology, Vol: 8
Gillet NA, Hlela C, Verdonck T, et al., 2011, HTLV-1 clonality during chronic infection and BLV clonality during primary infection, Retrovirology, Vol: 8
Tattermusch S, Skinner J, Chaussabel D, et al., 2011, An interferon signature is associated with HAM/TSP but not viral containment in HTLV-1 infection, Retrovirology, Vol: 8
Rowan AG, Bangham CRM, 2011, Is there a role for HTLV-1-specific CTL in adult T-cell Leukemia/Lymphoma?, Leukemia Research and Treatment, Vol: 2012, ISSN: 2090-3219
ATLL is an aggressive malignancy of T cells that affects about 5% of individuals infected with HTLV-1. The precise mechanism of oncogenesis is not known, but there is evidence that two regulatory viral proteins, Tax and HBZ, are involved. A high set point proviral load is associated with development of ATLL or a chronic inflammatory condition, HAM/TSP. Several lines of evidence, including HLA class 1 association studies and in vitro killing assays, indicate that cytotoxic T lymphocytes are instrumental in determining this proviral load set point. Prior studies have focused chiefly on the CTL response to the immunodominant Tax protein: efficient lysis of Tax-expressing cells inversely correlates with proviral load in nonmalignant infection. However, a recent study showed that strong binding of peptides from HBZ, but not Tax, to HLA class 1 molecules was associated with a low proviral load and a reduced risk of developing HAM/TSP, indicating an important role for HBZ-specific CTL in determining infection outcome. In comparison with nonmalignant infection, HTLV-1-specific CTLs in ATLL patients are reduced in frequency and functionally deficient. Here we discuss the nature of protective CTL responses in nonmalignant HTLV-1 infection and explore the potential of CTLs to protect against ATLL.
Martin F, Bangham CRM, Ciminale V, et al., 2011, Conference highlights of the 15th international conference on human retrovirology: HTLV and related retroviruses, 4-8 june 2011, Leuven, Gembloux, Belgium, RETROVIROLOGY, Vol: 8, ISSN: 1742-4690
- Author Web Link
- Cite
- Citations: 11
Seich al Basatena NK, MacNamara A, Vine AM, et al., 2011, KIR2DL2 enhances protective and detrimental HLA class I-mediated immunity in chronic viral infection., PLoS Pathogens, Vol: 7
Killer cell immunoglobulin-like receptors (KIRs) influence both innate and adaptive immunity. But while the role of KIRs inNK-mediated innate immunity is well-documented, the impact of KIRs on the T cell response in human disease is not known. Here we test the hypothesis that an individual’s KIR genotype affects the efficiency of their HLA class I-mediated antiviral immune response and the outcome of viral infection. We show that, in two unrelated viral infections, hepatitis C virus and human T lymphotropic virus type 1, possession of the KIR2DL2 gene enhanced both protective and detrimental HLA class Irestrictedanti-viral immunity. These results reveal a novel role for inhibitory KIRs. We conclude that inhibitory KIRs, in synergy with T cells, are a major determinant of the outcome of persistent viral infection.
Kirk PDW, Witkover A, Courtney A, et al., 2011, Plasma proteome analysis in HTLV-1-associated myelopathy/tropical spastic paraparesis, Retrovirology, Vol: 8, ISSN: 1742-4690
Background: Human T lymphotropic virus Type 1 (HTLV-1) causes a chronic inflammatory disease of the central nervous system known as HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM) which resembles chronic spinal forms of multiple sclerosis (MS). The pathogenesis of HAM remains uncertain. To aid in the differential diagnosis of HAM and to identify pathogenetic mechanisms we analysed the plasma proteome in asymptomatic HTLV-1 carriers (ACs), patients with HAM, uninfected controls and patients with MS. We used surface-enhanced laser desorption-ionization (SELDI) mass spectrometry to analyse the plasma proteome in 68 HTLV-1-infected individuals (in two non-overlapping sets, each comprising 17 patients with HAM and 17 ACs), 16 uninfected controls, and 11 patients with secondary progressive MS. Candidate biomarkers were identified by tandem Q-TOF mass spectrometry. Results: The concentrations of three plasma proteins – high [2-microglobulin], high [Calgranulin B], and low [apolipoprotein A2] – were specifically associated with HAM, independently of proviral load. The plasma [2-microglobulin] was positively correlated with disease severity. Conclusions: The results indicate that monocytes are activated by contact with activated endothelium in HAM. Using 2-microglobulin and Calgranulin B alone we derive a diagnostic algorithm that correctly classified the disease status (presence or absence of HAM) in 81% of HTLV-1-infected subjects in the cohort.
Villaudy J, Wencker M, Gadot N, et al., 2011, HTLV-1 Propels Thymic Human T Cell Development in "Human Immune System" Rag2<SUP>-/-</SUP> gamma c<SUP>-/-</SUP> Mice, PLOS PATHOGENS, Vol: 7, ISSN: 1553-7366
- Author Web Link
- Open Access Link
- Cite
- Citations: 48
Thomas S, Xue S-A, Bangham CRM, et al., 2011, Human T cells expressing affinity-matured TCR display accelerated responses but fail to recognize low density of MHC-peptide antigen, BLOOD, Vol: 118, Pages: 319-329, ISSN: 0006-4971
- Author Web Link
- Cite
- Citations: 76
Rende F, Cavallari I, Corradin A, et al., 2011, Kinetics and intracellular compartmentalization of HTLV-1 gene expression: nuclear retention of <i>HBZ</i> mRNAs, BLOOD, Vol: 117, Pages: 4855-4859, ISSN: 0006-4971
- Author Web Link
- Cite
- Citations: 81
Gillet N, Malani N, Melamed A, et al., 2011, Host genomic environment determines HTLV-1 clone size <i>in vivo</i>, CANCER RESEARCH, Vol: 71, ISSN: 0008-5472
Gillet NA, Malani N, Melamed A, et 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
- Author Web Link
- Cite
- Citations: 222
Hilburn S, Rowan A, Demontis M-A, et al., 2011, In vivo Expression of Human T-lymphotropic Virus Type 1 Basic Leucine-Zipper Protein Generates Specific CD8+and CD4+T-Lymphocyte Responses that Correlate with Clinical Outcome, JOURNAL OF INFECTIOUS DISEASES, Vol: 203, Pages: 529-536, ISSN: 0022-1899
- Author Web Link
- Open Access Link
- Cite
- Citations: 53
Bangham CRM, 2011, HTLV-1, Encyclopedia of Life Sciences
Human T lymphotropic virus Type 1 (HTLV-1) was the first human retrovirus discovered. Like the related virus HIV-1, HTLV-1 persists lifelong in the host. But whereas HIV-1 causes disease in over 99% of untreated infected people, HTLV-1 causes disease in only 2% to 8%: either a fatal leukaemia or lymphoma, or a disabling chronic inflammatory disease of the nervous system that causes paralysis of the legs. There is no satisfactory treatment for the malignant or inflammatory diseases, and no vaccine. HTLV-1 is thought to have existed in the human population for over 50 thousand years; it is widely but unevenly distributed in the tropics and in some sub-tropical areas. A highly dynamic equilibrium is established in each infected person between persistent HTLV-1 replication and the host immune response. The increasing understanding of this equilibrium has led to discoveries and conclusions of wide significance for virology, immunology and persistent infections.
Bangham CRM, Toulza F, 2011, Adult T Cell Leukemia/Lymphoma: FoxP3<SUP>+</SUP> Cells and the Cell-Mediated Immune Response to HTLV-1, ADVANCES IN CANCER RESEARCH, VOL 111, Vol: 111, Pages: 163-182, ISSN: 0065-230X
- Author Web Link
- Cite
- Citations: 23
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.