Relevant bibliographies by topics / Retrovirus HTLV

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Reports

Academic literature on the topic 'Retrovirus HTLV'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Retrovirus HTLV"

1

Zheng, Z. Y., and D. Zucker-Franklin. "Apparent ineffectiveness of natural killer cells vis-à-vis retrovirus-infected targets." Journal of Immunology 148, no. 11 (June 1, 1992): 3679–85. http://dx.doi.org/10.4049/jimmunol.148.11.3679.

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Abstract The role of NK cells in the defense against retroviral infections is ill defined. The discovery of the pathogenic human retroviruses and their epidemic spread have made more urgent a better understanding of how such infections may be naturally controlled. Therefore, a systematic study was undertaken to determine whether NK cells obtained from healthy individuals are able to recognize and lyse target cells that have been infected with HTLV-I, HTLV-II, or HIV. The studies demonstrated that NK cells can recognize retrovirus-infected cells as evidenced by rapid conjugation, but that neither freshly isolated, nor IL-2 stimulated cells cause lysis of such targets. As has been reported for NK-resistant tumor cells, removal of sialic acid residues rendered the retrovirus-infected target cells vulnerable to NK cell attack. Although these data do not suggest that boosting natural immunity would be a useful treatment modality for patients with AIDS or HTLV-related diseases, the observations may help to explain why the small number of cells that harbor retroviruses in patients with subclinical infection are not eliminated.
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Magin, Christine, Roswitha Löwer, and Johannes Löwer. "cORF and RcRE, the Rev/Rex and RRE/RxRE Homologues of the Human Endogenous Retrovirus Family HTDV/HERV-K." Journal of Virology 73, no. 11 (November 1, 1999): 9496–507. http://dx.doi.org/10.1128/jvi.73.11.9496-9507.1999.

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ABSTRACT cORF, a protein encoded by the human endogenous retrovirus family HTDV/HERV-K, contains amino acid motifs which resemble the nuclear import and export signals of the viral regulatory proteins Rev (human immunodeficiency virus) and Rex (human T-cell leukemia virus [HTLV]). In this study, we demonstrated that cORF indeed has a Rev-like function and mapped the cORF-responsive RNA element to a sequence in the 3′ long terminal repeat, a localization similar to RxRE, the responsive element in HTLV type 1. Accordingly, we have given the element the designation RcRE. cORF and RcRE stabilize unspliced and incompletely spliced viral transcripts and enhance their nuclear export via the CRM1 export pathway. So far, HTDV/HERV-K is the only endogenous retrovirus family with a complex regulation at the posttranscriptional level. It may be regarded as an intermediate in the evolution from simple to complex retroviruses.
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Cleveland, Susan M., and Utpal P. Dave. "Insertional Activation of GLI2 in Adult T-Cell Leukemia/Lymphoma." Blood 110, no. 11 (November 16, 2007): 4149. http://dx.doi.org/10.1182/blood.v110.11.4149.4149.

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Abstract Retroviruses induce cancer by integrating into the cellular genome and activating oncogenes or inactivating tumor suppressor genes. Human T-cell Leukemia Virus type 1 (HTLV-1), a complex retrovirus, induces Adult T-cell Leukemia/Lymphoma (ATLL) after a latency of over 30 years and in only 5% of carriers. The long latency and incomplete penetrance is similar to how slow transforming retroviruses induce cancer in mice and imply multiple oncogenic “hits” need to accumulate for clinically apparent disease. Insertional mutagenesis may be one mechanism by which ATLL develops. We used splinkerette-PCR to clone and map insertion sites from an HTLV-1 infected T-cell line, Hut-102. We identified an HTLV-1 insertion 5′ of the GLI2 gene, formerly known as Tax-Helper-Protein-1. We found GLI2 was up-regulated by promoter insertion. Interestingly, we found GLI2 protein occupied the HTLV-1 Long Terminal Repeat. The effect of GLI2 expression on viral expression was investigated by knockdown of GLI2 in Hut-102 cells. Our results show that retroviral insertional mutagenesis can be an important mechanism in HTLV-1-induced leukemias and lymphomas.
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Braoudaki, Maria, and Fotini Tzortzatou-Stathopoulou. "Tumorigenesis related to retroviral infections." Journal of Infection in Developing Countries 5, no. 11 (November 10, 2011): 751–58. http://dx.doi.org/10.3855/jidc.1773.

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Retroviral infections are considered important risk factors for cancer development in humans since approximately 15-20% of cancer worldwide is caused by an infectious agent. This report discusses the most established oncogenic retroviruses, including human immunodeficiency virus (HIV), human T-cell leukemia virus (HTLV-1 and -2), Rous sarcoma virus (RSV), Abelson murine leukemia virus (A-MuLV), Moloney murine leukemia virus (M-MuLV), murine mammary tumor virus (MMTV), bovine leukemia virus, (BLV), Jaagsiekte sheep retrovirus (JSRV), and Friend spleen focus-forming virus (SFFV). The role of retroviruses as inducers of carcinogenesis, the mechanisms underlying oncogenic transformation, and the routes of transmission of several cancer-related retroviral infections are also described. Finally, the impact of cancer-related retroviral infections in the developing world is addressed. This review is an update of carcinogenesis caused by retroviral infections.
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Hanson, Heather M., Nora A. Willkomm, Huixin Yang, and Louis M. Mansky. "Human Retrovirus Genomic RNA Packaging." Viruses 14, no. 5 (May 19, 2022): 1094. http://dx.doi.org/10.3390/v14051094.

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Two non-covalently linked copies of the retrovirus genome are specifically recruited to the site of virus particle assembly and packaged into released particles. Retroviral RNA packaging requires RNA export of the unspliced genomic RNA from the nucleus, translocation of the genome to virus assembly sites, and specific interaction with Gag, the main viral structural protein. While some aspects of the RNA packaging process are understood, many others remain poorly understood. In this review, we provide an update on recent advancements in understanding the mechanism of RNA packaging for retroviruses that cause disease in humans, i.e., HIV-1, HIV-2, and HTLV-1, as well as advances in the understanding of the details of genomic RNA nuclear export, genome translocation to virus assembly sites, and genomic RNA dimerization.
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Larkin, Julie, John T. Sinnott, Joshua Weiss, and Douglas A. Holt. "Human T-Cell Lymphotropic Virus-Type I." Infection Control & Hospital Epidemiology 11, no. 6 (June 1990): 314–18. http://dx.doi.org/10.1086/646177.

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Human T-cell lymphotropic virus type-1 (HTLV-I) is a recently recognized retrovirus identified as the cause of adult T-cell leukemia-lymphoma (ATLL) and HTLV-I-associated myelopathy (TSPI HAM). HTLV-I, a member of theRetroviridaefamily of viruses, was first described in 1980 after the isolation of the virus from a patient with a T-cell lymphoma. These pathogenic retroviruses are typically divided into theOncovirinaeandLentivirinae. The oncovirus group, including HTLV-I, HTLV-II and bovine leukemia virus (BLV), is generally associated with tumors. The lentiviruses are associated with immune deficiency and/or neurologic disease, and include agents such as the visna virus of sheep and the human immunodeficiency virus type-1 and -2 HIV-1 and HIV-2).
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Cohen, Isaac, and Jules E. Harris. "HTLV-I: The forgotten retrovirus." Medical and Pediatric Oncology 16, no. 1 (1988): 48–56. http://dx.doi.org/10.1002/mpo.2950160112.

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Fujita, M., K. Murata, and H. Shiku. "Selective inhibition of human T-lymphotropic virus type I-transformed human T-cell growth by a tax-targeted conditionally cytotoxic recombinant retrovirus." Blood 84, no. 8 (October 15, 1994): 2591–96. http://dx.doi.org/10.1182/blood.v84.8.2591.2591.

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Abstract Adult T-cell leukemia (ATL), a disorder associated with high mortality rates, arises from human T-lymphotropic virus type I (HTLV-I)-infected CD4+ T cells. We designed a retroviral vector-based gene therapy approach to ATL. The long terminal repeat (LTR) of HTLV-I is transactivated by the viral tax protein. We constructed a hybrid gene consisting of herpes simplex virus thymidine kinase (HSV TK) under the control of the HTLV-I LTR and inserted it into a retroviral vector. When HTLV-I-transformed and tax-expressing human T-cell lines were infected with this recombinant retrovirus (LNLTK alpha virus), they expressed high levels of HSV TK and exhibited increased sensitivity to acyclovir, a nucleoside analog that is converted to the toxic anabolite after phosphorylation by the HSV TK. On the other hand, the retroviral infection had little effect on acyclovir-induced cytotoxicity in HTLV-I- negative human hematopoietic cell lines. Our data may provide the prospect of the gene therapy for ATL by tax-targeted selective elimination of leukemic cells.
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Fujita, M., K. Murata, and H. Shiku. "Selective inhibition of human T-lymphotropic virus type I-transformed human T-cell growth by a tax-targeted conditionally cytotoxic recombinant retrovirus." Blood 84, no. 8 (October 15, 1994): 2591–96. http://dx.doi.org/10.1182/blood.v84.8.2591.bloodjournal8482591.

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Adult T-cell leukemia (ATL), a disorder associated with high mortality rates, arises from human T-lymphotropic virus type I (HTLV-I)-infected CD4+ T cells. We designed a retroviral vector-based gene therapy approach to ATL. The long terminal repeat (LTR) of HTLV-I is transactivated by the viral tax protein. We constructed a hybrid gene consisting of herpes simplex virus thymidine kinase (HSV TK) under the control of the HTLV-I LTR and inserted it into a retroviral vector. When HTLV-I-transformed and tax-expressing human T-cell lines were infected with this recombinant retrovirus (LNLTK alpha virus), they expressed high levels of HSV TK and exhibited increased sensitivity to acyclovir, a nucleoside analog that is converted to the toxic anabolite after phosphorylation by the HSV TK. On the other hand, the retroviral infection had little effect on acyclovir-induced cytotoxicity in HTLV-I- negative human hematopoietic cell lines. Our data may provide the prospect of the gene therapy for ATL by tax-targeted selective elimination of leukemic cells.
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Satou, Yorifumi, Paola Miyazato, Ko Ishihara, Hiroko Yaguchi, Anat Melamed, Michi Miura, Asami Fukuda, et al. "The retrovirus HTLV-1 inserts an ectopic CTCF-binding site into the human genome." Proceedings of the National Academy of Sciences 113, no. 11 (February 29, 2016): 3054–59. http://dx.doi.org/10.1073/pnas.1423199113.

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Human T-lymphotropic virus type 1 (HTLV-1) is a retrovirus that causes malignant and inflammatory diseases in ∼10% of infected people. A typical host has between 104 and 105 clones of HTLV-1–infected T lymphocytes, each clone distinguished by the genomic integration site of the single-copy HTLV-1 provirus. The HTLV-1 bZIP (HBZ) factor gene is constitutively expressed from the minus strand of the provirus, whereas plus-strand expression, required for viral propagation to uninfected cells, is suppressed or intermittent in vivo, allowing escape from host immune surveillance. It remains unknown what regulates this pattern of proviral transcription and latency. Here, we show that CTCF, a key regulator of chromatin structure and function, binds to the provirus at a sharp border in epigenetic modifications in the pX region of the HTLV-1 provirus in T cells naturally infected with HTLV-1. CTCF is a zinc-finger protein that binds to an insulator region in genomic DNA and plays a fundamental role in controlling higher order chromatin structure and gene expression in vertebrate cells. We show that CTCF bound to HTLV-1 acts as an enhancer blocker, regulates HTLV-1 mRNA splicing, and forms long-distance interactions with flanking host chromatin. CTCF-binding sites (CTCF-BSs) have been propagated throughout the genome by transposons in certain primate lineages, but CTCF binding has not previously been described in present-day exogenous retroviruses. The presence of an ectopic CTCF-BS introduced by the retrovirus in tens of thousands of genomic locations has the potential to cause widespread abnormalities in host cell chromatin structure and gene expression.
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Dissertations / Theses on the topic "Retrovirus HTLV"

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MAHIEUX, RENAUD. "De la diversite genetique des retrovirus htlv-i et stlv-i." Paris 6, 1997. http://www.theses.fr/1997PA066447.

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La variabilite genetique du virus htlv-i a ete etudiee par plusieurs approches complementaires : - les travaux d'epidemiologie moleculaire ont permis d'une part de decrire un nouveau sous-type d'htlv-i (htlv-i d) present en afrique centrale, d'autre part de montrer que la repartition des sous-types viraux presents en afrique est liee au moins a 3 facteurs : a) l'origine geographique des souches virales b) des transmissions singes-hommes repetees, c) l'evolution genetique lente du virus dans des populations isolees. Par ailleurs, un nouveau stlv-i a ete caracterise au niveau moleculaire chez macaca arctoides, singe qui presentait une serologie htlv indeterminee. Ce nouveau virus de la famille des htlv-i/stlv-i est le plus divergent connu actuellement et sa decouverte suggere qu'il devrait exister des virus htlv-i aussi divergents dans certaines populations du sud-est asiatique. Enfin, l'absence de mutation associee a une pathologie donnee (atl ou tsp/ham) a ete confirmee pour une region de la proteine tax. - l'etude des quasiespeces d'htlv-i apres l'infection de singes saimiri sciureus a montre que la faible variabilite genomique observee etait probablement le reflet d'une faible replication virale meme dans cette espece simienne naive pour les stlvs. La stabilite genetique observee chez cet animal serait donc due a la biologie du virus qui ne lui permet pas de se repliquer efficacement et ce quel que soit l'hote infecte. - concernant le mecanisme moleculaire qui regit la faible variabilite genetique d'htlv-i observee in vivo, nous avons montre que la transcriptase inverse d'htlv-i pouvait aussi commettre des erreurs mais a un niveau moindre que celle de vih-1. - la presence d'un virus apparente a htlv-i a ete recherchee dans des populations d'afrique chez lesquelles on trouve frequemment un profil de western-blot indetermine proche de celui retrouve chez les individus infectes par htlv-i. Aucune sequence htlv-i n'a pu etre detectee dans les cellules mononucleees du sang peripherique de ces personnes et nos resultats suggerent que ces profils indetermines pourraient etre dus a des seroreactivites croisees contre certains antigenes palustres qui restent a definir.
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Rosenberg, Arielle. "Les glycoproteines d'enveloppe des retrovirus htlv-1 et htlv-2 : de la maturation intracellulaire aux fonctions dans la transmission virale." Paris 6, 1999. http://www.theses.fr/1999PA066441.

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Synthetisees dans la cellule infectee, les glycoproteines d'enveloppe des retrovirus gouvernent l'entree virale dans une nouvelle cellule cible. En adoptant les retrovirus htlv comme modeles d'etude, cette these analyse l'oligomerisation des glycoproteines d'enveloppe tout le long de leur existence, depuis leur maturation intracellulaire dans la cellule infectee jusqu'aux evenements qui conduisent a la transmission retrovirale dans une cellule cible. Dans la premiere partie du travail, j'a mis au point un test d'infectivite qui permet d'etudier la transmission des retrovirus htlv au cours d'un seul cycle d'infection. Puis, par mutagenese dirigee, j'ai defini la contribution des differentes regions des proteines d'enveloppe a leur maturation et a leurs fonctions. J'ai ainsi etabli la validite des glycoproteines de htlv comme modeles d'etude des glycoproteines retrovirales. Dans la seconde partie du travail, j'ai combine deux approches experimentales complementaires pour etudier l'oligomerisation des glycoproteines d'enveloppe : des tests fonctionnels qui etudient le caractere transdominant de mutants d'enveloppe, et des tests biochimiques qui mettent en evidence les oligomeres de glycoproteines. D'une part, j'ai montre que l'oligomerisation du precurseur d'enveloppe dans le reticulum endoplasmique requiert l'integrite du domaine n-terminal, et propose que l'assemblage des proteines survient precocement au cours du processus de maturation intracellulaire, ce qui favoriserait le repliement cooperatif de monomeres. D'autre part, j'ai etabli que chacune des etapes du processus d'entree necessite que les glycoproteines d'enveloppe soient sous forme d'oligomeres. Mes resultats suggerent que l'activation de la fusion virale ferait intervenir une transition dans l'ordre d'oligomerisation des glycoproteines, d'une forme dimerique - forme mature mais non-fusiogene presente a la surface de cellules infectees et des virions - a une forme trimerique - effectrice de la fusion.
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Le, Guern Fellous Muriel. "Détection par amplification génique du génome HTLV dans différentes symptomatologies." Paris 5, 1989. http://www.theses.fr/1989PA05P060.

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Silverman, Lee. "Role of human T-lymphotropic virus type 1 p30(II) and surface envelope as determinants of in vivo pathogenesis." Connect to this title online, 2005. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1108502317.

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Thesis (Ph. D.)--Ohio State University, 2005.
Title from first page of PDF file. Document formatted into pages; contains xvii, 216 p.; also includes graphics (some col.). Includes bibliographical references. Available online via OhioLINK's ETD Center
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Le, Blanc-Louvry Isabelle. "Role des proteines gag du retrovirus htlv-1 dans la formation d'un virus infectueux." Paris 7, 2000. http://www.theses.fr/2000PA077129.

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Le travail realise au cours de cette these visait a comprendre le role des proteines gag du retrovirus htlv-1 dans la formation d'un virus infectieux. Comme pour les autres retrovirus, ces proteines forment l'architecture interne du virus, et gouvernent l'assemblage et le bourgeonnement de nouveaux virions depuis la membrane des cellules infectees. Les proteines gag sont synthetisees sous la forme d'une polyproteine, le precurseur gag, qui est ensuite clive par la protease virale en produits matures : matrice, capside et nucleocapside. Afin etudier le trafic intracellulaire du precurseur gag d'htlv-1 depuis son lieu de synthese cytoplasmique jusqu'a la membrane plasmique ou debute le bourgeonnement, nous avons realise une etude systematique de colocalisation avec les compartiments membranaires intracellulaires. Nos resultats indiquent que le transport de gag a la membrane plasmique est independant des membranes intracellulaires mais necessite l'integrite du cytosquelette d'actine. Afin de definir les motifs proteiques qui, dans la matrice de htlv-1, sont necessaires a l'infection, nous avons introduit des mutations dans cette proteine et teste leur effet sur la maturation des proteines gag, la morphogenese et la production des particules virales, et l'infectivite du virus. Nous avons montre que les acides amines basiques de la matrice d'htlv-1 sont necessaires a de multiples fonctions, incluant non seulement la production de particules virales, mais aussi des evenements precoces du cycle viral qui sont requis pour une infection efficace de nouvelles cellules cibles. D'autre part, nous avons etabli que le motif pppy de la matrice d'htlv-1 est implique dans une etape precoce du bourgeonnement. La comparaison de nos resultats
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Trentin, Bernadette. "Transcriptase inverse du HTLV-I : expression, structure et rôle dans l'infectiosité/." Bordeaux 2, 1999. http://www.theses.fr/1999BOR28640.

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Kawatsuki, Akihiro. "HTLV-1 bZIP factor protein targets the Rb/E2F-1 pathway to promote proliferation and apoptosis of primary CD4+ T cells." Kyoto University, 2016. http://hdl.handle.net/2433/215441.

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The author’s accepted version (the unedited manuscript) may be deposited into a repository six months after print publication. In this case, authors should cite the publication reference and DOI number on any deposited version, and provide a link from it to the published article on the NPG website.
Kyoto University (京都大学)
0048
新制・課程博士
博士(医学)
甲第19615号
医博第4122号
新制||医||1015(附属図書館)
32651
京都大学大学院医学研究科医学専攻
(主査)教授 生田 宏一, 教授 松田 道行, 教授 高田 穣
学位規則第4条第1項該当
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Goetz, Michael. "Etudes structurales et analyse de l'antigénicité de la glycoprotéine de surface du retrovirus humain HTLV-I." Bordeaux 1, 1996. http://www.theses.fr/1996BOR10627.

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Le retrovirus htlv-i (human t-cell leukemia virus type i) est associe a deux pathologies graves chez l'homme, la leucemie a cellules t de l'adulte et la paraparesie spastique tropicale. Sa glycoproteine de surface (gp46) est impliquee dans les evenements precoces de l'infection virale. Ce travail s'insere dans le cadre de l'elaboration d'une strategie vaccinale, et propose une double approche d'analyse de la gp46. La structure en solution de fragments peptidiques de synthese est etudiee par dichroisme circulaire et par resonance magnetique nucleaire bidimensionnelle du proton. L'antigenicite de la region immunodominante 239-261 de la gp46 est analysee en fonction de la variabilite de sa sequence proteique ; dans cette region, nous avons defini plusieurs epitopes reconnus par des anticorps contenus dans les serums de patients htlv-i positifs. Les premiers resultats des tests d'immunisation de lapins avec un prototype de vaccin synthetique sont presentes
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Lanigan, Lisa Gooding. "Effects of Two Cancer Genes, HTLV-1 Tax and E-Cadherin, on Cancer Development and Progression." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1339177362.

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El, Dassouki Zeina. "Ciblage thérapeutique de l'oncoprotéine virale Tax dans les Leucémies/Lymphomes T de l'adulte (ATL) associées au retrovirus HTLV-I." Paris 7, 2014. http://www.theses.fr/2014PA077093.

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L'ATL est une prolifération tumorale de cellules lymphoïdes T matures activées ; cette maladie est caractérisée par un mauvais pronostic, du fait d'une resistance importante à la chimiothérapie conventionnelle. L'oncoprotéine TAX joue un rôle primordial dans la prolifération et la transformation des lymphocytes infectées par HTLV-1. Notre équipe a montré que l'arsenic synergise avec l'interferon pour induire dans les cellules leucémiques infectées, un arrêt du cycle cellulaire, une apoptose massive ainsi qu'une dégradation proteosomique spécifique de TAX. Cette dégradation semble être à la base de l'élimination des cellules initiatrices de leucémie (CIL) et l'éradication de l'ATL. Néanmoins, les mécanismes moléculaires du ciblage de TAX par l'arsenic/IFN restaient élusifs. Mon projet de thèse a eu pour objectif d'élucider ces mécanismes. Dans mon travail de thèse, nous avons confirmé, pour la première fois, que la survie des lignées cellulaires dérivées d'ATL est dépendante de l'expression continue de TAX indiquant la contribution majeure de la dégradation de cette oncoprotéine dans la réponse thérapeutique. De plus, la dégradation de TAX sous l'effet de l'arsenic/IFN est due à sa sumoylation et à son ubiquitination séquentielle, médiées par PML et RNF4 respectivement. Ces résultats ont permis de proposer un modèle sur l'effet de l'arsenic/IFN sur les modifications post-traductionnelles de TAX et les enzymes qui y sont impliqués. Par conséquent, le renforcement des CNS suivi par la dégradation des protéines symoylées pathogènes, par un traitement ciblé, pourrait avoir un large intéret thérapeutique
The HTLV-1 TAX Transactivator initiates transformation in adult T-cell leukemia/Lymphoma (ATL), a highly aggressive chemotherapy-resistant malignancy. The arsenic/Interferon combination, which triggers degradation of the tax oncoprotein, selectively precipates apoptosis of ATL cell lines and cures TAX-driven murine ATL. Yet, the role of tax loss in ATL response is disputed and the molecular mechanisms driving degradation remain elusive. Here we demonstrate that ATL-derived cells are addicted to continuous tax expression, implying that tax degradation underlies clinical responses to the arsenic/interferon combination in mice and patients. The latter enforces PML nuclear body (NB) formation and partner protein recruitment. In arsenic/interferon-treated ATL cells, TAX is recruited onto NBS, undergoes PML-dependent hyper-sumoylation by SUMO2/3,but not SUMO1, ubiquitination by RNF4 and proteasome-dependent degradation. Thus arsenic/Interferon is a targeted therapy of ATL, enforcing NB formation by arsenic/Interferon therapy could have broad therapeutic value to destroy pathogenic sumoylated proteins
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Books on the topic "Retrovirus HTLV"

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C, Gallo Robert, and Jay Gilbert, eds. The Human retroviruses. San Diego: Academic Press, 1991.

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Dani, Bolognesi, Abbott Laboratories, University of California, Los Angeles., and Abbott-UCLA Symposium on Human Retroviruses, Cancer, and AIDS: Approaches to Prevention and Therapy (1987 : Keystone, Colo.), eds. Human retroviruses, cancer and AIDS: Approaches to prevention and therapy : proceedings of an Abbott-UCLA Symposium held at Keystone, Colorado, April 1-6, 1987. New York: Liss, 1988.

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Bryan, Cullen, ed. Human retroviruses. Oxford: IRL Press at Oxford University Press, 1993.

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Yoshiki, Takashi. Molecular pathology of human retroviruses, HTLV-I and endogenous retroviruses. Sapporo, Japan: Hokkaido University Graduate School of Medicine, 2004.

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Schüpbach, Jörg. Human retrovirology: Facts and concepts. Berlin: Springer-Verlag, 1989.

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Human retrovirology: Facts and concepts. Berlin: Springer-Verlag, 1990.

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Schüpbach, Jörg. Human retrovirology: Facts and concepts. Berlin: Springer-Verlag, 1989.

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Y, Chen Irvin S., ed. Transacting functions of human retroviruses. Berlin: Springer-Verlag, 1995.

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Center for Drugs and Biologics (U.S.), ed. Compliance program reference: Inspections of licensed and unlicensed blood banks (compliance program #7342.001) and inspections of source plasma establishments (compliance program #7342.002). [Rockville, MD]: Center for Drugs and Biologics, 1985.

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E, Groopman Jerome, and University of California, Los Angeles., eds. Human retroviruses: Proceedings of a Chimertech-UCLA symposium, held at Tamarron, Colorado, February 4-11, 1989. New York: Wiley-Liss, 1990.

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Book chapters on the topic "Retrovirus HTLV"

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Greenberg, Steven J. "HTLV Retrovirus in Neurological Disease." In PCR Topics, 147–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75924-6_29.

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Lairmore, Michael D., and Renu Lal. "Other Human Retrovirus Infections: HTLV-I and HTLV-II." In AIDS Testing, 168–88. New York, NY: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4684-0514-9_12.

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Levine, Alexandra M., Parkash Gill, Paul Meyer, and Suraiya Rasheed. "Human T-Lymphotropic Retrovirus (HTLV-III) Associated Lymphoproliferative Disorders in Homosexual Men." In Lymphoproliferative Diseases: Pathogenesis, Diagnosis, Therapy, 191–203. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5016-0_15.

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Forlani, Greta, Roberto S. Accolla, and Giovanna Tosi. "Investigating Human T Cell Lymphotropic Retrovirus (HTLV) Tax Function with Molecular and Immunophenotypic Techniques." In Methods in Molecular Biology, 299–313. Totowa, NJ: Humana Press, 2014. http://dx.doi.org/10.1007/978-1-62703-670-2_24.

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Närvänen, A., M. Korkolainen, F. Lillo, O. Varnier, R. Rescaldani, A. Visconti, E. De Gourville, A. Vaheri, and M. L. Huhtala. "Synthetic Peptides Derived from HIV-1, HIV-2, and HTLV-I Envelope Proteins in Human Retrovirus Serology." In Rapid Methods and Automation in Microbiology and Immunology, 123–30. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76603-9_15.

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Sugamura, Kazuo, and Yorio Hinuma. "Human Retroviruses: HTLV-I and HTLV-II." In The Retroviridae, 399–435. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4899-1627-3_7.

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Hatanaka, M., and S. H. Nam. "Synthesis and Activity of HTLV-1 Protease and its Muteins." In Proteases of Retroviruses, edited by Vladimír Kostka, 119–24. Berlin, Boston: De Gruyter, 1989. http://dx.doi.org/10.1515/9783110862782-015.

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8

Khabbaz, Rima F., Walid Heneine, and Jonathan E. Kaplan. "Testing for Other Human Retroviruses: HTLV-I and HTLV-II." In AIDS Testing, 206–23. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-0867-9_11.

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Yoshida, M., T. Suzuki, J. Fujisawa, and H. Hirai. "HTLV-1 Oncoprotein Tax and Cellular transcription Factors." In Transacting Functions of Human Retroviruses, 79–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-78929-8_4.

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Wong-Staal, F. "Molecular Biology of Viruses of the HTLV Family." In International Symposium: Retroviruses and Human Pathology, 265–73. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-5008-1_24.

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Reports on the topic "Retrovirus HTLV"

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Kanki, Phyllis J. Characterization of African Human Retroviruses Related to HTLV-III/LAV. Fort Belvoir, VA: Defense Technical Information Center, June 1988. http://dx.doi.org/10.21236/ada199785.

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