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Journal articles on the topic 'HTLV-1 Tax'

Author: Grafiati

Published: 4 June 2021

Last updated: 2 February 2022

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1

Yamano, Yoshihisa, Masahiro Nagai, Meghan Brennan, et al. "Correlation of human T-cell lymphotropic virus type 1 (HTLV-1) mRNA with proviral DNA load, virus-specific CD8+ T cells, and disease severity in HTLV-1–associated myelopathy (HAM/TSP)." Blood 99, no. 1 (2002): 88–94. http://dx.doi.org/10.1182/blood.v99.1.88.

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To investigate the role of viral expression in individuals infected with human T-cell lymphotropic virus type 1 (HTLV-1), a real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) of HTLV-1 tax messenger RNA (mRNA) using ABI Prism 7700 Sequence Detection System was developed. Using this system, the HTLV-1tax mRNA load was compared with HTLV-1 proviral DNA load, HTLV-1 Tax protein expression, HTLV-1 Tax-specific CD8+T-cell frequency, and disease severity of HTLV-1–associated myelopathy/tropical spastic paraparesis (HAM/TSP). This approach was a sensitive and specific tec

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2

Boxus, Mathieu, Jean-Claude Twizere, Sébastien Legros, Jean-François Dewulf, Richard Kettmann, and Luc Willems. "The HTLV-1 Tax interactome." Retrovirology 5, no. 1 (2008): 76. http://dx.doi.org/10.1186/1742-4690-5-76.

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3

Tang, Hei-Man Vincent, Wei-Wei Gao, Chi-Ping Chan, et al. "SIRT1 Suppresses Human T-Cell Leukemia Virus Type 1 Transcription." Journal of Virology 89, no. 16 (2015): 8623–31. http://dx.doi.org/10.1128/jvi.01229-15.

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ABSTRACTHuman T-cell leukemia virus type 1 (HTLV-1)-associated diseases are poorly treatable, and HTLV-1 vaccines are not available. High proviral load is one major risk factor for disease development. HTLV-1 encodes Tax oncoprotein, which activates transcription from viral long terminal repeats (LTR) and various types of cellular promoters. Counteracting Tax function might have prophylactic and therapeutic benefits. In this work, we report on the suppression of Tax activation of HTLV-1 LTR by SIRT1 deacetylase. The transcriptional activity of Tax on the LTR was largely ablated when SIRT1 was

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4

Mahieux, Renaud, Cynthia A. Pise-Masison, Paul F. Lambert, et al. "Differences in the Ability of Human T-Cell Lymphotropic Virus Type 1 (HTLV-1) and HTLV-2 Tax To Inhibit p53 Function." Journal of Virology 74, no. 15 (2000): 6866–74. http://dx.doi.org/10.1128/jvi.74.15.6866-6874.2000.

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ABSTRACT We have analyzed the functional activity of the p53 tumor suppressor in human T-cell lymphotropic virus type 2 (HTLV-2)-transformed cells. Abundant levels of the p53 protein were detected in both HTLV-2A and -2B virus-infected cell lines. The p53 was functionally inactive, however, both in transient-transfection assays using a p53 reporter plasmid and in induction of p53-responsive genes in response to gamma irradiation. We further investigated HTLV-2A Tax and HTLV-2B Tax effects on p53 activity. Interestingly, although Tax-2A and -2B inactivate p53, the Tax-2A protein appears to inhi

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5

Lu, Hanxin, Cynthia A. Pise-Masison, Rebecca Linton, et al. "Tax Relieves Transcriptional Repression by Promoting Histone Deacetylase 1 Release from the Human T-Cell Leukemia Virus Type 1 Long Terminal Repeat." Journal of Virology 78, no. 13 (2004): 6735–43. http://dx.doi.org/10.1128/jvi.78.13.6735-6743.2004.

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ABSTRACT Expression of human T-cell leukemia virus type 1 (HTLV-1) is regulated by the viral transcriptional activator Tax. Tax activates viral transcription through interaction with the cellular transcription factor CREB and the coactivators CBP/p300. In this study, we have analyzed the role of histone deacetylase 1 (HDAC1) on HTLV-1 gene expression from an integrated template. First we show that trichostatin A, an HDAC inhibitor, enhances Tax expression in HTLV-1-transformed cells. Second, using a cell line containing a single-copy HTLV-1 long terminal repeat, we demonstrate that overexpress

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6

Xie, Li, Brenda Yamamoto, Abdelali Haoudi, O. John Semmes, and Patrick L. Green. "PDZ binding motif of HTLV-1 Tax promotes virus-mediated T-cell proliferation in vitro and persistence in vivo." Blood 107, no. 5 (2006): 1980–88. http://dx.doi.org/10.1182/blood-2005-03-1333.

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HTLV-1 cellular transformation and disease induction is dependent on expression of the viral Tax oncoprotein. PDZ is a modular protein interaction domain used in organizing signaling complexes in eukaryotic cells through recognition of a specific binding motif in partner proteins. Tax-1, but not Tax-2, contains a PDZ-binding domain motif (PBM) that promotes the interaction with several cellular PDZ proteins. Herein, we investigate the contribution of the Tax-1 PBM in HTLV-induced proliferation and immortalization of primary T cells in vitro and viral survival in an infectious rabbit animal mod

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7

Ku, Sebastian C. Y., Jialing Lee, Joanne Lau, et al. "XBP-1, a Novel Human T-Lymphotropic Virus Type 1 (HTLV-1) Tax Binding Protein, Activates HTLV-1 Basal and Tax-Activated Transcription." Journal of Virology 82, no. 9 (2008): 4343–53. http://dx.doi.org/10.1128/jvi.02054-07.

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ABSTRACT X-box binding protein 1 (XBP-1), a basic leucine zipper transcription factor, plays a key role in the cellular unfolded protein response (UPR). There are two XBP-1 isoforms in cells, spliced XBP-1S and unspliced XBP-1U. XBP-1U has been shown to bind to the 21-bp Tax-responsive element of the human T-lymphotropic virus type 1 (HTLV-1) long terminal repeat (LTR) in vitro and transactivate HTLV-1 transcription. Here we identify XBP-1S as a transcription activator of HTLV-1. Compared to XBP-1U, XBP-1S demonstrates stronger activating effects on both basal and Tax-activated HTLV-1 transcri

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8

Dezzutti, Charlene S., Patricia C. Guenthner, Sylvester Daniel, et al. "Detection of Human T-Lymphotropic Virus (HTLV) tax Sequences in New York City Blood Donors Seronegative for HTLV Types 1 and 2." Clinical Diagnostic Laboratory Immunology 10, no. 4 (2003): 715–17. http://dx.doi.org/10.1128/cdli.10.4.715-717.2003.

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ABSTRACT A potential public health concern is the reported detection of the human T-lymphotropic virus (HTLV) tax gene in the lymphocytes of up to 11% of a low-risk group of New York City blood donors (NYBD). This study aimed to independently confirm the prevalence of HTLV tax sequences in 293 NYBD. All NYBD tested negative for antibodies to HTLV types 1 and 2 and HTLV Tax. HTLV tax sequences were not detected in the NYBD lymphocytes. These data demonstrate the lack of HTLV-1 tax in this group of NYBD at low risk for HTLV infection.

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9

Tsukada, Junichi, Takehiro Higashi, Atsushi Iwashige, et al. "Lipopolysaccharide(LPS)-Induction of the HTLV-1 LTR in Monocytes." Blood 118, no. 21 (2011): 2167. http://dx.doi.org/10.1182/blood.v118.21.2167.2167.

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Abstract Abstract 2167 The human leukemia virus type 1 (HTLV-1) gene expression is regulated by the viral proteins and various cellular transcription factors. HTLV-1 genome encodes not only structural proteins, but also non-structural proteins such as Tax, a transcriptional activator for STAT5 p12I, and HTLV-1 bZIP factor (HBZ) encoded by the minus strand of the viral genome. The functional analysis of the viral proteins such as Tax has shed light on the pathogenesis of adult T cell leukemia/lymphoma (ATL). Expression of Tax is enhanced by T-cell activation stimuli such as phorbol ester (PMA),

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10

Mohanty, Suchitra, and Edward W. Harhaj. "Mechanisms of Oncogenesis by HTLV-1 Tax." Pathogens 9, no. 7 (2020): 543. http://dx.doi.org/10.3390/pathogens9070543.

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The human T-cell lymphotropic virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATLL), a neoplasm of CD4+CD25+ T cells that occurs in 2–5% of infected individuals after decades of asymptomatic latent infection. Multiple HTLV-1-encoded regulatory proteins, including Tax and HTLV-1 basic leucine zipper factor (HBZ), play key roles in viral persistence and latency. The HTLV-1 Tax oncoprotein interacts with a plethora of host cellular proteins to regulate viral gene expression and also promote the aberrant activation of signaling pathways such as NF-κB to drive clon

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11

Zucker-Franklin, Dorothea, Bette A. Pancake, Parviz Lalezari, and Manoochehr Khorshidi. "Transmission of Human T-Cell Lymphotropic Virus Type 1 Tax to Rabbits by tax-Only-Positive Human Cells." Clinical Diagnostic Laboratory Immunology 7, no. 2 (2000): 274–78. http://dx.doi.org/10.1128/cdli.7.2.274-278.2000.

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ABSTRACT The human T-cell lymphrotropic virus type 1 (HTLV-1) is causally related to adult T-cell leukemia and lymphoma and the neurodegenerative diseases tropical spastic paraparesis and HTLV-1-associated myelopathy. In the United States the prevalence of infection has been estimated to range from 0.016 to 0.1% on the basis of serologic tests for antibodies to the viral structural proteins. Blood from donors positive for antibodies to HTLV-1 or HTLV-2 is not used for transfusion. However, patients with the cutaneous T-cell lymphoma mycosis fungoides (MF) are HTLV-1 and -2 seronegative yet har

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12

Lin, Hsin-Ching, Charlene S. Dezzutti, Renu B. Lal, and Arnold B. Rabson. "Activation of Human T-Cell Leukemia Virus Type 1tax Gene Expression in Chronically Infected T Cells." Journal of Virology 72, no. 7 (1998): 6264–70. http://dx.doi.org/10.1128/jvi.72.7.6264-6270.1998.

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ABSTRACT Expression of human T-cell leukemia virus type 1 (HTLV-1) is regulated both by the HTLV-1 Tax transactivator and by cellular transcriptional factors binding to the viral long terminal repeat (LTR), suggesting that cellular signals may play a role in regulating viral expression. Treatment of cells chronically infected with HTLV-1, which express low levels of HTLV-1 RNAs and Tax protein, with phorbol esters (i.e., phorbol12-myristate 13- acetate [PMA]), phytohemagglutinin (PHA), sodium butyrate, or combinations of cytokines resulted in induction of HTLV- 1 gene expression. PMA or PHA tr

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13

Shirinian, Margret, Zakaria Kambris, Lama Hamadeh, et al. "A Transgenic Drosophila melanogaster Model To Study Human T-Lymphotropic Virus Oncoprotein Tax-1-Driven TransformationIn Vivo." Journal of Virology 89, no. 15 (2015): 8092–95. http://dx.doi.org/10.1128/jvi.00918-15.

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Human T-cell lymphotropic virus type 1 (HTLV-1)-induced adult T-cell leukemia/lymphoma is an aggressive malignancy. HTLV-2 is genetically related to HTLV-1 but does not cause any malignant disease. HTLV-1 Tax transactivator (Tax-1) contributes to leukemogenesis via NF-κB. We describe transgenicDrosophilamodels expressing Tax in the compound eye and plasmatocytes. We demonstrate that Tax-1 but not Tax-2 induces ommatidial perturbation and increased plasmatocyte proliferation and that the eye phenotype is dependent on Kenny (IKKγ/NEMO), thus validating this newin vivomodel.

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14

Liu, Meihong, Liangpeng Yang, Ling Zhang, et al. "Human T-Cell Leukemia Virus Type 1 Infection Leads to Arrest in the G1 Phase of the Cell Cycle." Journal of Virology 82, no. 17 (2008): 8442–55. http://dx.doi.org/10.1128/jvi.00091-08.

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ABSTRACT Infection by the human T-cell leukemia virus type 1 (HTLV-1) is thought to cause dysregulated T-cell proliferation, which in turn leads to adult T-cell leukemia/lymphoma. Early cellular changes after HTLV-1 infection have been difficult to study due to the poorly infectious nature of HTLV-1 and the need for cell-to-cell contact for HTLV-1 transmission. Using a series of reporter systems, we show that HeLa cells cease proliferation within one or two division cycles after infection by HTLV-1 or transduction of the HTLV-1 tax gene. HTLV-1-infected HeLa cells, like their tax-transduced co

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15

Belrose, Gildas, Antoine Gross, Stéphane Olindo, et al. "Effects of valproate on Tax and HBZ expression in HTLV-1 and HAM/TSP T lymphocytes." Blood 118, no. 9 (2011): 2483–91. http://dx.doi.org/10.1182/blood-2010-11-321364.

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AbstractA determinant of human T-lymphotropic virus-1 (HTLV-1)–associated myelopathy/tropical spastic paraparesis (HAM/TSP) development is the HTLV-1–infected cell burden. Viral proteins Tax and HBZ, encoded by the sense and antisense strands of the pX region, respectively, play key roles in HTLV-1 persistence. Tax drives CD4+-T cell clonal expansion and is the immunodominant viral antigen recognized by the immune response. Valproate (2-n-propylpentanoic acid, VPA), a histone deacetylase inhibitor, was thought to trigger Tax expression, thereby exposing the latent HTLV-1 reservoir to immune de

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16

Ye, Jianxin, Li Xie, and Patrick L. Green. "Tax and Overlapping Rex Sequences Do Not Confer the Distinct Transformation Tropisms of Human T-Cell Leukemia Virus Types 1 and 2." Journal of Virology 77, no. 14 (2003): 7728–35. http://dx.doi.org/10.1128/jvi.77.14.7728-7735.2003.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are distinct oncogenic retroviruses that infect several cell types but display their biological and pathogenic activity only in T cells. Previous studies have indicated that in vivo HTLV-1 has a preferential tropism for CD4+ T cells, whereas HTLV-2 in vivo tropism is less clear but appears to favor CD8+ T cells. Both CD4+ and CD8+ T cells are susceptible to HTLV-1 and HTLV-2 infection in vitro, and HTLV-1 has a preferential immortalization and transformation tropism of CD4+ T cells, whereas HTLV-2 immortalizes and transforms prima

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17

Sabouri, Amir H., Mineki Saito, Koichiro Usuku, et al. "Differences in viral and host genetic risk factors for development of human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis between Iranian and Japanese HTLV-1-infected individuals." Journal of General Virology 86, no. 3 (2005): 773–81. http://dx.doi.org/10.1099/vir.0.80509-0.

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Human T-cell lymphotropic virus type 1 (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a neurological disease observed only in 1–2 % of infected individuals. HTLV-1 provirus load, certain HLA alleles and HTLV-1 tax subgroups are reported to be associated with different levels of risk for HAM/TSP in Kagoshima, Japan. Here, it was determined whether these risk factors were also valid for HTLV-1-infected individuals in Mashhad in northeastern Iran, another region of endemic HTLV-1 infection. In Iranian HTLV-1-infected individuals (n=132, 58 HAM/TSP patients and 74 seropos

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18

LEE, SUNG-JI, JI SHIN LEE, MYUNG-GEUN SHIN, et al. "Detection of HTLV-1 in the Labial Salivary Glands of Patients with Sjögren’s Syndrome: A Distinct Clinical Subgroup?" Journal of Rheumatology 39, no. 4 (2012): 809–15. http://dx.doi.org/10.3899/jrheum.111075.

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Objective.To examine whether patients with Sjögren’s syndrome (SS) can be distinguished based on the expression of human T cell lymphotrophic virus type I (HTLV-1) and, if so, whether the subgroups differ in their clinical features and serological measures.Methods.Polymerase chain reaction (PCR) and nested PCR were used to amplify viral DNA from peripheral blood mononuclear cells (PBMC) in 53 patients with SS, using primers from the HTLV-1 pX, p19, pol, and tax regions. Minor salivary gland biopsy specimens from 33 patients with SS were examined for the presence of HTLV-1 p19 or tax proteins i

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Pise-Masison, Cynthia A., Kyeong-Sook Choi, Michael Radonovich, Jürgen Dittmer, Seong-Jin Kim, and John N. Brady. "Inhibition of p53 Transactivation Function by the Human T-Cell Lymphotropic Virus Type 1 Tax Protein." Journal of Virology 72, no. 2 (1998): 1165–70. http://dx.doi.org/10.1128/jvi.72.2.1165-1170.1998.

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ABSTRACT Human T-cell lymphotropic virus type 1 (HTLV-1) is the etiologic agent for adult T-cell leukemia. HTLV-1 transforms lymphocytes, and there is increasing evidence that the virus-encoded protein, Tax, plays a primary role in viral transformation. We have shown that wild-type p53 in HTLV-1-transformed cells is stabilized. This study was initiated to directly analyze whether the p53 in HTLV-1-transformed cell lines was transcriptionally active and to identify the viral gene product responsible for stabilization and inactivation. Transfection experiments using a p53-responsive reporter pla

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20

Schnell, Annika P., Stephan Kohrt, and Andrea K. Thoma-Kress. "Latency Reversing Agents: Kick and Kill of HTLV-1?" International Journal of Molecular Sciences 22, no. 11 (2021): 5545. http://dx.doi.org/10.3390/ijms22115545.

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Human T-cell leukemia virus type 1 (HTLV-1), the cause of adult T-cell leukemia/lymphoma (ATLL), is a retrovirus, which integrates into the host genome and persistently infects CD4+ T-cells. Virus propagation is stimulated by (1) clonal expansion of infected cells and (2) de novo infection. Viral gene expression is induced by the transactivator protein Tax, which recruits host factors like positive transcription elongation factor b (P-TEFb) to the viral promoter. Since HTLV-1 gene expression is repressed in vivo by viral, cellular, and epigenetic mechanisms in late phases of infection, HTLV-1

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21

Tomita, Mariko, Akira Kikuchi, Tetsu Akiyama, Yuetsu Tanaka та Naoki Mori. "Human T-Cell Leukemia Virus Type 1 Tax Dysregulates β-CateninSignaling". Journal of Virology 80, № 21 (2006): 10497–505. http://dx.doi.org/10.1128/jvi.00739-06.

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ABSTRACT Dysregulation of β-catenin signaling has been implicated in the malignant transformation of cells. However, the role of β-catenin in the human T-cell leukemia virus type 1 (HTLV-1)-induced transformation of T cells is unknown. Here we found that β-catenin protein was overexpressed in the nucleus and that β-catenin-dependent transcription was significantly enhanced in Tax-positive HTLV-1-infected T-cell lines compared to that in Tax-negative HTLV-1-infected T-cell lines. Transfection withβ -catenin-specific small interfering RNA inhibited the growth of the Tax-positive HTLV-1-infected

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22

Andresen, Vibeke, Cynthia A. Pise-Masison, Uma Sinha-Datta, et al. "Suppression of HTLV-1 replication by Tax-mediated rerouting of the p13 viral protein to nuclear speckles." Blood 118, no. 6 (2011): 1549–59. http://dx.doi.org/10.1182/blood-2010-06-293340.

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AbstractDisease development in human T-cell leukemia virus type 1 (HTLV-1)–infected individuals is positively correlated with the level of integrated viral DNA in T cells. HTLV-1 replication is positively regulated by Tax and Rex and negatively regulated by the p30 and HBZ proteins. In the present study, we demonstrate that HTLV-1 encodes another negative regulator of virus expression, the p13 protein. Expressed separately, p13 localizes to the mitochondria, whereas in the presence of Tax, part of it is ubiquitinated, stabilized, and rerouted to the nuclear speckles. The p13 protein directly b

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23

Elovaara, I., S. Koenig, A. Y. Brewah, R. M. Woods, T. Lehky, and S. Jacobson. "High human T cell lymphotropic virus type 1 (HTLV-1)-specific precursor cytotoxic T lymphocyte frequencies in patients with HTLV-1-associated neurological disease." Journal of Experimental Medicine 177, no. 6 (1993): 1567–73. http://dx.doi.org/10.1084/jem.177.6.1567.

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The frequencies of human T cell lymphotropic virus type 1 (HTLV-1)-specific CD8+ precursor cytotoxic T lymphocytes (pCTL) were quantitated from lymphocytes obtained from the peripheral blood and cerebrospinal fluid (CSF) of infected individuals with and without HTLV-1-associated neurological disease. An estimate of the pCTL was obtained by separating CD8+ cells, plating these cells in limiting dilution, and testing wells for HTLV-1 specific lysis. Targets consisted of autologous lymphoblastoid cell lines (LCL) infected with vaccinia constructs expressing HTLV-1 gene products or LCL pulsed with

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Kress, Andrea K., Grit Schneider, Klemens Pichler, Martina Kalmer, Bernhard Fleckenstein, and Ralph Grassmann. "Elevated Cyclic AMP Levels in T Lymphocytes Transformed by Human T-Cell Lymphotropic Virus Type 1." Journal of Virology 84, no. 17 (2010): 8732–42. http://dx.doi.org/10.1128/jvi.00487-10.

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ABSTRACT Human T-cell lymphotropic virus type 1 (HTLV-1), the cause of adult T-cell leukemia/lymphoma (ATLL), transforms CD4+ T cells to permanent growth through its transactivator Tax. HTLV-1-transformed cells share phenotypic properties with memory and regulatory T cells (T-reg). Murine T-reg-mediated suppression employs elevated cyclic AMP (cAMP) levels as a key regulator. This led us to determine cAMP levels in HTLV-1-transformed cells. We found elevated cAMP concentrations as a consistent feature of all HTLV-1-transformed cell lines, including in vitro-HTLV-1-transformed, Tax-transformed,

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Ohashi, Takashi, Shino Hanabuchi, Hirotomo Kato, et al. "Prevention of Adult T-Cell Leukemia-Like Lymphoproliferative Disease in Rats by Adoptively Transferred T Cells from a Donor Immunized with Human T-Cell Leukemia Virus Type 1 Tax-Coding DNA Vaccine." Journal of Virology 74, no. 20 (2000): 9610–16. http://dx.doi.org/10.1128/jvi.74.20.9610-9616.2000.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL) in infected individuals after a long incubation period. To dissect the mechanisms of the development of the disease, we have previously established a rat model of ATL-like disease which allows examination of the growth and spread of HTLV-1 infected tumor cells, as well assessment of the effects of immune T cells on the development of the disease. In the present study, we induced HTLV-1 Tax-specific cytotoxic T lymphocyte (CTL) immunity by vaccination with Tax-coding DNA and examined the effects of the DNA v

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Younis, Ihab, Lyne Khair, Miroslav Dundr, Michael D. Lairmore, Genoveffa Franchini, and Patrick L. Green. "Repression of Human T-Cell Leukemia Virus Type 1 and Type 2 Replication by a Viral mRNA-Encoded Posttranscriptional Regulator." Journal of Virology 78, no. 20 (2004): 11077–83. http://dx.doi.org/10.1128/jvi.78.20.11077-11083.2004.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) and HTLV-2 are complex retroviruses that persist in the host, eventually causing leukemia and neurological disease in a small percentage of infected individuals. In addition to structural and enzymatic proteins, HTLV encodes regulatory (Tax and Rex) and accessory (open reading frame I and II) proteins. The viral Tax and Rex proteins positively regulate virus production. Tax activates viral and cellular transcription to promote T-cell growth and, ultimately, malignant transformation. Rex acts posttranscriptionally to facilitate cytoplasmic ex

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Jeong, Soo-Jin, Hanxin Lu, Won-Kyung Cho, Hyeon Ung Park, Cynthia Pise-Masison, and John N. Brady. "Coactivator-Associated Arginine Methyltransferase 1 Enhances Transcriptional Activity ofthe Human T-Cell Lymphotropic Virus Type 1 Long Terminal Repeat through Direct Interactionwith Tax." Journal of Virology 80, no. 20 (2006): 10036–44. http://dx.doi.org/10.1128/jvi.00186-06.

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ABSTRACT In this study, we demonstrate that the coactivator-associated arginine methyltransferase 1 (CARM1), which methylates histone H3 and other proteins such as p300/CBP, is positively involved in the regulation of Tax transactivation. First, transfection studies demonstrated that overexpression of CARM1 wild-type protein resulted in increased Tax transactivation of the human T-cell lymphotropic virus type 1 (HTLV-1) long terminal repeat (LTR). In contrast, transfection of a catalytically inactive CARM1 methyltransferase mutant did not enhance Tax transactivation. CARM1 facilitated Tax tran

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Twizere, Jean-Claude, Jean-Yves Springael, Mathieu Boxus, et al. "Human T-cell leukemia virus type-1 Tax oncoprotein regulates G-protein signaling." Blood 109, no. 3 (2006): 1051–60. http://dx.doi.org/10.1182/blood-2006-06-026781.

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AbstractHuman T-cell leukemia virus type-1 (HTLV-1) is associated with adult T-cell leukemia (ATL) and neurological syndromes. HTLV-1 encodes the oncoprotein Tax-1, which modulates viral and cellular gene expression leading to T-cell transformation. Guanine nucleotide–binding proteins (G proteins) and G protein–coupled receptors (GPCRs) constitute the largest family of membrane proteins known and are involved in the regulation of most biological functions. Here, we report an interaction between HTLV-1 Tax oncoprotein and the G-protein β subunit. Interestingly, though the G-protein β subunit in

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Fochi, Stefania, Vincenzo Ciminale, Elisabetta Trabetti та ін. "NF-κB and MicroRNA Deregulation Mediated by HTLV-1 Tax and HBZ". Pathogens 8, № 4 (2019): 290. http://dx.doi.org/10.3390/pathogens8040290.

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The risk of developing adult T-cell leukemia/lymphoma (ATLL) in individuals infected with human T-cell lymphotropic virus 1 (HTLV-1) is about 3–5%. The mechanisms by which the virus triggers this aggressive cancer are still an area of intensive investigation. The viral protein Tax-1, together with additional regulatory proteins, in particular HTLV-1 basic leucine zipper factor (HBZ), are recognized as relevant viral factors required for both viral replication and transformation of infected cells. Tax-1 deregulates several cellular pathways affecting the cell cycle, survival, and proliferation.

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Mulloy, J. C., T. Kislyakova, A. Cereseto, et al. "Human T-Cell Lymphotropic/Leukemia Virus Type 1 Tax Abrogates p53-Induced Cell Cycle Arrest and Apoptosis through Its CREB/ATF Functional Domain." Journal of Virology 72, no. 11 (1998): 8852–60. http://dx.doi.org/10.1128/jvi.72.11.8852-8860.1998.

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ABSTRACT Human T-cell lymphotropic/leukemia virus type 1 (HTLV-1) transforms human T cells in vitro, and Tax, a potent transactivator of viral and cellular genes, plays a key role in cell immortalization. Tax activity is mediated by interaction with cellular transcription factors including members of the CREB/ATF family, the NF-κB/c-Rel family, serum response factor, and the coactivators CREB binding protein-p300. Although p53 is usually not mutated in HTLV-1-infected T cells, its half-life is increased and its function is impaired. Here we report that transient coexpression of p53 and Tax res

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Kozako, Tomohiro, Masaki Akimoto, Izumi Masamoto, et al. "The Frequency, Diversity, and Function of Human T-Cell Leukemia Virus Type 1-Specific CD8+ T-Cell Is Reduced in Adult T-Cell Leukemia Patients." Blood 108, no. 11 (2006): 1264. http://dx.doi.org/10.1182/blood.v108.11.1264.1264.

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Abstract Human T-cell lymphotropic virus type 1 (HTLV-1)-specific CTL are thought to be immune effectors that reduce the risk of adult T-cell leukemia (ATL). However, in vivo conditions of anti-HTLV-1 CTL before and after ATL development have yet to be determined. To characterize anti-HTLV-1 CTL in asymptomatic HTLV-1 carriers (AC) and ATL patients, we analyzed the frequency and diversity of HTLV-1-specific CD8+ T cells in PBMC of 35 AC and 32 ATL patients using 16 distinct epitopes of HTLV-1 Tax or Env/HLA tetramers along with intracellular cytolytic effector molecules (IFN-γ , perforin, and

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Nomura, Machiko, Takashi Ohashi, Keiko Nishikawa, et al. "Repression of Tax Expression Is Associated both with Resistance of Human T-Cell Leukemia Virus Type 1-Infected T Cells to Killing by Tax-Specific Cytotoxic T Lymphocytes and with Impaired Tumorigenicity in a Rat Model." Journal of Virology 78, no. 8 (2004): 3827–36. http://dx.doi.org/10.1128/jvi.78.8.3827-3836.2004.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL). Although the viral transactivation factor, Tax, has been known to have apparent transforming ability, the exact function of Tax in ATL development is still not clear. To understand the role of Tax in ATL development, we introduced short-interfering RNAs (siRNAs) against Tax in a rat HTLV-1-infected T-cell line. Our results demonstrated that expression of siRNA targeting Tax successfully downregulated Tax expression. Repression of Tax expression was associated with resistance of the HTLV-1-infected T cells

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Wäldele, Katja, Grit Schneider, Tobias Ruckes, and Ralph Grassmann. "Interleukin-13 Overexpression by Tax Transactivation: a Potential Autocrine Stimulus in Human T-Cell Leukemia Virus-Infected Lymphocytes." Journal of Virology 78, no. 12 (2004): 6081–90. http://dx.doi.org/10.1128/jvi.78.12.6081-6090.2004.

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ABSTRACT The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein induces growth transformation and is critical for the pathogenesis of the HTLV-1-induced adult T-cell leukemia (ATL). It stimulates the cell cycle and transactivates cellular genes. Here we show that the expression of interleukin-13 (IL-13) is upregulated as a consequence of Tax in HTLV-1-transformed T cells and ATL-derived cultures. IL-13 exerts proliferative and antiapoptotic functions and is linked to leukemogenesis, since it stimulates Hodgkin lymphoma cells by an autocrine mechanism. Overexpression of IL-13 RNA and p

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Moriuchi, Masako, and Hiroyuki Moriuchi. "Induction of Lactoferrin Gene Expression in Myeloid or Mammary Gland Cells by Human T-Cell Leukemia Virus Type 1 (HTLV-1) Tax: Implications for Milk-Borne Transmission of HTLV-1." Journal of Virology 80, no. 14 (2006): 7118–26. http://dx.doi.org/10.1128/jvi.00409-06.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1), the causative agent of adult T-cell leukemia, is transmitted vertically via breastfeeding. We have previously demonstrated that lactoferrin, a major milk protein, enhances HTLV-1 replication, at least in part by upregulating the HTLV-1 long terminal repeat promoter. We now report that HTLV-1 infection can induce lactoferrin gene expression. Coculture with HTLV-1-infected MT-2 cells increased the levels of lactoferrin mRNA in myeloid-differentiated HL-60 cells, as well as MCF-7 cells, models of two probable sources (neutrophils and mammary e

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Ozden, Simona, Vincent Mouly, Marie-Christine Prevost, Antoine Gessain, Gillian Butler-Browne, and Pierre-Emmanuel Ceccaldi. "Muscle Wasting Induced by HTLV-1 Tax-1 Protein." American Journal of Pathology 167, no. 6 (2005): 1609–19. http://dx.doi.org/10.1016/s0002-9440(10)61245-x.

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Tang, Sai-Wen, Chia-Yen Chen, Zachary Klase, Linda Zane, and Kuan-Teh Jeang. "The Cellular Autophagy Pathway Modulates Human T-Cell Leukemia Virus Type 1 Replication." Journal of Virology 87, no. 3 (2012): 1699–707. http://dx.doi.org/10.1128/jvi.02147-12.

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ABSTRACTAutophagy, a general homeostatic process for degradation of cytosolic proteins or organelles, has been reported to modulate the replication of many viruses. The role of autophagy in human T-cell leukemia virus type 1 (HTLV-1) replication has, however, been uncharacterized. Here, we report that HTLV-1 infection increases the accumulation of autophagosomes and that this accumulation increases HTLV-1 production. We found that the HTLV-1 Tax protein increases cellular autophagosome accumulation by acting to block the fusion of autophagosomes to lysosomes, preventing the degradation of the

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Goon, Peter K. C., Emmanuel Hanon, Tadahiko Igakura, et al. "High frequencies of Th1-type CD4+ T cells specific to HTLV-1 Env and Tax proteins in patients with HTLV-1–associated myelopathy/tropical spastic paraparesis." Blood 99, no. 9 (2002): 3335–41. http://dx.doi.org/10.1182/blood.v99.9.3335.

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Abstract CD4+ T cells are critical for inducing and maintaining efficient humoral and cellular immune responses to pathogens. The CD4+ T-cell response in human T-lymphotropic virus 1 (HTLV-1) infection has not been studied in detail. However, CD4+ T cells have been shown to predominate in early lesions in HTLV-1–associated myelopathy/tropical spastic paraparesis (HAM/TSP). We present direct estimates of HTLV-1 Env- and Tax-specific CD4+ T-cell frequencies in patients infected with HTLV-1. We first showed that there was a strong bias toward the Th1 phenotype in these HTLV-1–specific CD4+ T cell

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Forlani, Greta, Rawan Abdallah, Roberto S. Accolla та Giovanna Tosi. "The Major Histocompatibility Complex Class II Transactivator CIITA Inhibits the Persistent Activation of NF-κB by the Human T Cell Lymphotropic Virus Type 1 Tax-1 Oncoprotein". Journal of Virology 90, № 7 (2016): 3708–21. http://dx.doi.org/10.1128/jvi.03000-15.

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ABSTRACTHuman T cell lymphotropic virus type 1 (HTLV-1) Tax-1, a key protein in HTLV-1-induced T cell transformation, deregulates diverse cell signaling pathways. Among them, the NF-κB pathway is constitutively activated by Tax-1, which binds to NF-κB proteins and activates the IκB kinase (IKK). Upon phosphorylation-dependent IκB degradation, NF-κB migrates into the nucleus, mediating Tax-1-stimulated gene expression. We show that the transcriptional regulator of major histocompatibility complex class II genes CIITA (class II transactivator), endogenously or ectopically expressed in different

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Raza, Md Thosif, Shagufta Mizan, Farhana Yasmin, Al-Shahriar Akash, and Shah Md Shahik. "Epitope-based universal vaccine for Human T-lymphotropic virus-1 (HTLV-1)." PLOS ONE 16, no. 4 (2021): e0248001. http://dx.doi.org/10.1371/journal.pone.0248001.

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Human T-cell leukemia virus type 1 (HTLV-1) was the first oncogenic human retrovirus identified in humans which infects at least 10–15 million people worldwide. Large HTLV-1 endemic areas exist in Southern Japan, the Caribbean, Central and South America, the Middle East, Melanesia, and equatorial regions of Africa. HTLV-1 TAX viral protein is thought to play a critical role in HTLV-1 associated diseases. We have used numerous bio-informatics and immuno-informatics implements comprising sequence and construction tools for the construction of a 3D model and epitope prediction for HTLV-1 Tax vira

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Enose-Akahata, Yoshimi, Nyater Ngouth, Joan Ohayon, et al. "Effect of Teriflunomide on Cells From Patients With Human T-cell Lymphotropic Virus Type 1–Associated Neurologic Disease." Neurology - Neuroimmunology Neuroinflammation 8, no. 3 (2021): e986. http://dx.doi.org/10.1212/nxi.0000000000000986.

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ObjectiveTo test the hypothesis that teriflunomide can reduce ex vivo spontaneous proliferation of peripheral blood mononuclear cells (PBMCs) from patients with human T-cell lymphotropic virus type 1 (HTLV-1)–associated myelopathy/tropical spastic paraparesis (HAM/TSP).MethodsPBMCs from patients with HAM/TSP were cultured in the presence and absence of teriflunomide and assessed for cell viability, lymphocyte proliferation, activation markers, HTLV-1 tax and HTLV-1 hbz messenger ribonucleic acid (mRNA) expression, and HTLV-1 Tax protein expression.ResultsIn culture, teriflunomide did not affec

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Dodon, Madeleine Duc, Zhenlin Li, Samir Hamaia, and Louis Gazzolo. "Tax protein of human T-cell leukaemia virus type 1 induces interleukin 17 gene expression in T cells." Journal of General Virology 85, no. 7 (2004): 1921–32. http://dx.doi.org/10.1099/vir.0.79921-0.

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Tax protein of human T-cell leukaemia virus type 1 (HTLV-1) induces the expression of several cellular genes that are involved in T cell activation and proliferation. In this study, it was observed that Tax upregulated the expression of human interleukin 17 (IL17), a cytokine mainly produced by activated CD4+ memory T cells. Indeed, IL17 mRNA was highly expressed in HTLV-1-infected T cells as well as in Tax-expressing Jurkat T cells, whereas it was not detectable in HTLV-1-negative T cell lines. The clinical relevance of these observations was further demonstrated by quantitative assessment of

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Chibueze, Ezinne Chioma, Yohann White, Makoto Yoshimitsu, et al. "Immune Exhaustion and 2B4 Expression in Human T-Cell Lymphotropic Virus Type 1(HTLV-1) Infection." Blood 120, no. 21 (2012): 4807. http://dx.doi.org/10.1182/blood.v120.21.4807.4807.

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Abstract Abstract 4807 Background: The role of the 2B4/CD48 pathway in chronic viral infections has been controversial, with some studies suggesting an enhancing and others an inhibitory effect on virus specific CD8 (+) cytotoxic T-lymphocytes. Human T-cell lymphotropic virus type 1 (HTLV-1) trans-activating (Tax) protein is crucial for viral replication and activates HTLV-1 gene transcription. Methods: Peripheral blood mononuclear cells (PBMCs) were isolated by Ficoll centrifugation and cryopreserved until use. For staining, cells were incubated with fluorochrome-conjugated antibodies against

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Mohanty, Suchitra, Teng Han, Young Bong Choi, Alfonso Lavorgna, Jiawen Zhang та Edward William Harhaj. "The E3/E4 ubiquitin conjugation factor UBE4B interacts with and ubiquitinates the HTLV-1 Tax oncoprotein to promote NF-κB activation". PLOS Pathogens 16, № 12 (2020): e1008504. http://dx.doi.org/10.1371/journal.ppat.1008504.

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Human T-cell leukemia virus type 1 (HTLV-1) is the etiological agent of adult T-cell leukemia/lymphoma (ATLL), and the neurological disease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 Tax protein persistently activates the NF-κB pathway to enhance the proliferation and survival of HTLV-1 infected T cells. Lysine 63 (K63)-linked polyubiquitination of Tax provides an important regulatory mechanism that promotes Tax-mediated interaction with the IKK complex and activation of NF-κB; however, the host proteins regulating Tax ubiquitination are largely unknown. To

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Masamoto, Izumi, Sawako Horai, Tomohiro Kozako, et al. "CD70 Expression on HTLV-1 Infected T Cells of Carriers and ATL Patients and Its Clinical Significance." Blood 116, no. 21 (2010): 1730. http://dx.doi.org/10.1182/blood.v116.21.1730.1730.

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Abstract Abstract 1730 Human T-lymphotropic virus type-1(HTLV-1) is the causative agent of adult T cell leukemia/lymphoma (ATL). HTLV-1 infected T cell growth or leukemogenesis in ATL is controlled by various host immune surveillance systems. Among them, CD70 on HTLV-1 infected T cells coupled with CD27 on virus specific cytotoxic T cells has been suggested to play an important role in ATL leukemogenesis. The CD70 molecule is the only known ligand for CD27, a member of the tumor necrosis factor (TNF) receptor superfamily 7. This negative immunoregulatory pathway downregulates cytotoxic T lymph

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Ohashi, Takashi, Shino Hanabuchi, Reiko Suzuki, Hirotomo Kato, Takao Masuda, and Mari Kannagi. "Correlation of Major Histocompatibility Complex Class I Downregulation with Resistance of Human T-Cell Leukemia Virus Type 1-Infected T Cells to Cytotoxic T-Lymphocyte Killing in a Rat Model." Journal of Virology 76, no. 14 (2002): 7010–19. http://dx.doi.org/10.1128/jvi.76.14.7010-7019.2002.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) causes adult T-cell leukemia (ATL) in infected individuals after a long incubation period. Despite the apparent transforming ability of HTLV-1 under experimental conditions, most HTLV-1 carriers are asymptomatic. These facts suggest that HTLV-1 is controlled by host immunity in most carriers. To understand the interplay between host immunity and HTLV-1-infected cells, in this study, we isolated several HTLV-1 Tax-specific cytotoxic T-lymphocyte (CTL) lines from rats inoculated with Tax-coding DNA and investigated the long-term effects of the

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Silbermann, Katrin, Grit Schneider та Ralph Grassmann. "Stimulation of interleukin-13 expression by human T-cell leukemia virus type 1 oncoprotein Tax via a dually active promoter element responsive to NF-κB and NFAT". Journal of General Virology 89, № 11 (2008): 2788–98. http://dx.doi.org/10.1099/vir.0.2008/003699-0.

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The human T-cell leukemia virus type 1 (HTLV-1) Tax oncoprotein transforms human lymphocytes and is critical for the pathogenesis of HTLV-1-induced adult T-cell leukaemia. In HTLV-transformed cells, Tax upregulates interleukin (IL)-13, a cytokine with proliferative and anti-apoptotic functions that is linked to leukaemogenesis. Tax-stimulated IL-13 is thought to result in autocrine stimulation of HTLV-infected cells and thus may be relevant to their growth. The causal transactivation of the IL-13 promoter by Tax is predominantly dependent on a nuclear factor of activated T cells (NFAT)-binding

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Toulza, Frederic, Adrian Heaps, Yuetsu Tanaka, Graham P. Taylor, and Charles R. M. Bangham. "High frequency of CD4+FoxP3+ cells in HTLV-1 infection: inverse correlation with HTLV-1–specific CTL response." Blood 111, no. 10 (2008): 5047–53. http://dx.doi.org/10.1182/blood-2007-10-118539.

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AbstractEvidence from population genetics, gene expression microarrays, and assays of ex vivo T-cell function indicates that the cytotoxic T lymphocyte (CTL) response to human T-lymphotropic virus type 1 (HTLV-1) controls the level of HTLV-1 expression and the proviral load. The rate at which CTLs kill autologous HTLV-1–infected lymphocytes differs significantly among infected people, but the reasons for such variation are unknown. Here, we demonstrate a strong negative cor-relation between the frequency of CD4+FoxP3+ Tax− regulatory T cells (Tregs) in the circulation and the rate of CTL-media

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Yuen, Chun-Kit, Ching-Ping Chan, Sin-Yee Fung, et al. "Suppression of Type I Interferon Production by Human T-Cell Leukemia Virus Type 1 Oncoprotein Tax through Inhibition of IRF3 Phosphorylation." Journal of Virology 90, no. 8 (2016): 3902–12. http://dx.doi.org/10.1128/jvi.00129-16.

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ABSTRACTInfection with human T-cell leukemia virus type 1 (HTLV-1) is associated with adult T-cell leukemia (ATL) and tropical spastic paraparesis. Type I interferons (IFNs) are key effectors of the innate antiviral response, and IFN-α combined with the nucleoside reverse transcriptase inhibitor zidovudine is considered the standard first-line therapy for ATL. HTLV-1 oncoprotein Tax is known to suppress innate IFN production and response but the underlying mechanisms remain to be fully established. In this study, we report on the suppression of type I IFN production by HTLV-1 Tax through inter

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Koya, Yoshihiro, Takashi Ohashi, Hirotomo Kato, et al. "Establishment of a Seronegative Human T-Cell Leukemia Virus Type 1 (HTLV-1) Carrier State in Rats Inoculated with a Syngeneic HTLV-1-Immortalized T-Cell Line Preferentially Expressing Tax." Journal of Virology 73, no. 8 (1999): 6436–43. http://dx.doi.org/10.1128/jvi.73.8.6436-6443.1999.

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ABSTRACT Human T-cell leukemia virus type 1 (HTLV-1) causes T-cell malignancies in a small percentage of the population infected with the virus after a long carrier state. In the present study, we established a seronegative HTLV-1 carrier state in rats inoculated with a newly established HTLV-1-infected rat T cell line, FPM1. FPM1 originated from rat thymocytes cocultured with a human HTLV-1 producer, MT-2 cells, and expressed rat CD4, CD5, CD25, and HTLV-1 Tax. However, FPM1 scarcely expressed other major HTLV-1 structural proteins and failed to induce typical antibody responses against HTLV-

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Younis, Ihab, Kathleen Boris-Lawrie, and Patrick L. Green. "Human T-Cell Leukemia Virus Open Reading Frame II Encodes a Posttranscriptional Repressor That Is Recruited at the Level of Transcription." Journal of Virology 80, no. 1 (2006): 181–91. http://dx.doi.org/10.1128/jvi.80.1.181-191.2006.

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ABSTRACT Human T-cell leukemia virus (HTLV) infection is a chronic, lifelong infection that is associated with the development of leukemia and neurological disease after a long latency period, and the mechanism by which the virus is able to evade host immune surveillance is elusive. Besides the structural and enzymatic proteins, HTLV encodes regulatory (Tax and Rex) and accessory (open reading frame I [ORF I] and ORF II) proteins. Tax activates viral and cellular transcription and promotes T-cell growth and malignant transformation. Rex acts posttranscriptionally to facilitate cytoplasmic expr

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