Relevant bibliographies by topics / Retrovirus transcription

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  2. Dissertations / Theses
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Academic literature on the topic 'Retrovirus transcription'

Author: Grafiati
Published: 11 March 2023

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Journal articles on the topic "Retrovirus transcription"

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Plachý, Jiří, Jan Kotáb, Petr Divina, Markéta Reinišová, Filip Šenigl, and Jiří Hejnar. "Proviruses Selected for High and Stable Expression of Transduced Genes Accumulate in Broadly Transcribed Genome Areas." Journal of Virology 84, no. 9 (February 10, 2010): 4204–11. http://dx.doi.org/10.1128/jvi.02511-09.

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ABSTRACT Retroviruses and retrovirus-derived vectors integrate nonrandomly into the genomes of host cells with specific preferences for transcribed genes, gene-rich regions, and CpG islands. However, the genomic features that influence the transcriptional activities of integrated retroviruses or retroviral vectors are poorly understood. We report here the cloning and characterization of avian sarcoma virus integration sites from chicken tumors. Growing progressively, dependent on high and stable expression of the transduced v-src oncogene, these tumors represent clonal expansions of cells bearing transcriptionally active replication-defective proviruses. Therefore, integration sites in our study distinguished genomic loci favorable for the expression of integrated retroviruses and gene transfer vectors. Analysis of integration sites from avian sarcoma virus-induced tumors showed strikingly nonrandom distribution, with proviruses found prevalently within or close to transcription units, particularly in genes broadly expressed in multiple tissues but not in tissue-specifically expressed genes. We infer that proviruses integrated in these genomic areas efficiently avoid transcriptional silencing and remain active for a long time during the growth of tumors. Defining the differences between unselected retroviral integration sites and sites selected for long-terminal-repeat-driven gene expression is relevant for retrovirus-mediated gene transfer and has ramifications for gene therapy.
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Schlesinger, Sharon, and Stephen P. Goff. "Retroviral Transcriptional Regulation and Embryonic Stem Cells: War and Peace." Molecular and Cellular Biology 35, no. 5 (December 29, 2014): 770–77. http://dx.doi.org/10.1128/mcb.01293-14.

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Retroviruses have evolved complex transcriptional enhancers and promoters that allow their replication in a wide range of tissue and cell types. Embryonic stem (ES) cells, however, characteristically suppress transcription of proviruses formed after infection by exogenous retroviruses and also of most members of the vast array of endogenous retroviruses in the genome. These cells have unusual profiles of transcribed genes and are poised to make rapid changes in those profiles upon induction of differentiation. Many of the transcription factors in ES cells control both host and retroviral genes coordinately, such that retroviral expression patterns can serve as markers of ES cell pluripotency. This overlap is not coincidental; retrovirus-derived regulatory sequences are often used to control cellular genes important for pluripotency. These sequences specify the temporal control and perhaps “noisy” control of cellular genes that direct proper cell gene expression in primitive cells and their differentiating progeny. The evidence suggests that the viral elements have been domesticated for host needs, reflecting the wide-ranging exploitation of any and all available DNA sequences in assembling regulatory networks.
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Evans, Leonard H., A. S. M. Alamgir, Nick Owens, Nick Weber, Kimmo Virtaneva, Kent Barbian, Amenah Babar, Frank Malik, and Kyle Rosenke. "Mobilization of Endogenous Retroviruses in Mice after Infection with an Exogenous Retrovirus." Journal of Virology 83, no. 6 (December 30, 2008): 2429–35. http://dx.doi.org/10.1128/jvi.01926-08.

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ABSTRACT Mammalian genomes harbor a large number of retroviral elements acquired as germ line insertions during evolution. Although many of the endogenous retroviruses are defective, several contain one or more intact viral genes that are expressed under certain physiological or pathological conditions. This is true of the endogenous polytropic retroviruses that generate recombinant polytropic murine leukemia viruses (MuLVs). In these recombinants the env gene sequences of exogenous ecotropic MuLVs are replaced with env gene sequences from an endogenous polytropic retrovirus. Although replication-competent endogenous polytropic retroviruses have not been observed, the recombinant polytropic viruses are capable of replicating in numerous species. Recombination occurs during reverse transcription of a virion RNA heterodimer comprised of an RNA transcript from an endogenous polytropic virus and an RNA transcript from an exogenous ecotropic MuLV RNA. It is possible that homodimers corresponding to two full-length endogenous RNA genomes are also packaged. Thus, infection by an exogenous virus may result not only in recombination with endogenous sequences, but also in the mobilization of complete endogenous retrovirus genomes via pseudotyping within exogenous retroviral virions. We report that the infection of mice with an ecotropic virus results in pseudotyping of intact endogenous viruses that have not undergone recombination. The endogenous retroviruses infect and are integrated into target cell genomes and subsequently replicate and spread as pseudotyped viruses. The mobilization of endogenous retroviruses upon infection with an exogenous retrovirus may represent a major interaction of exogenous retroviruses with endogenous retroviruses and may have profound effects on the pathogenicity of retroviral infections.
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Pluta, Aneta, Juan P. Jaworski, and César N. Cortés-Rubio. "Balance between Retroviral Latency and Transcription: Based on HIV Model." Pathogens 10, no. 1 (December 29, 2020): 16. http://dx.doi.org/10.3390/pathogens10010016.

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The representative of the Lentivirus genus is the human immunodeficiency virus type 1 (HIV-1), the causative agent of acquired immunodeficiency syndrome (AIDS). To date, there is no cure for AIDS because of the existence of the HIV-1 reservoir. HIV-1 infection can persist for decades despite effective antiretroviral therapy (ART), due to the persistence of infectious latent viruses in long-lived resting memory CD4+ T cells, macrophages, monocytes, microglial cells, and other cell types. However, the biology of HIV-1 latency remains incompletely understood. Retroviral long terminal repeat region (LTR) plays an indispensable role in controlling viral gene expression. Regulation of the transcription initiation plays a crucial role in establishing and maintaining a retrovirus latency. Whether and how retroviruses establish latency and reactivate remains unclear. In this article, we describe what is known about the regulation of LTR-driven transcription in HIV-1, that is, the cis-elements present in the LTR, the role of LTR transcription factor binding sites in LTR-driven transcription, the role of HIV-1-encoded transactivator protein, hormonal effects on virus transcription, impact of LTR variability on transcription, and epigenetic control of retrovirus LTR. Finally, we focus on a novel clustered regularly interspaced short palindromic repeats-associated protein 9 (CRISPR/dCas9)-based strategy for HIV-1 reservoir purging.
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Dimcheff, Derek E., Mallika Krishnan, and David P. Mindell. "Evolution and Characterization of Tetraonine Endogenous Retrovirus: a New Virus Related to Avian Sarcoma and Leukosis Viruses." Journal of Virology 75, no. 4 (February 15, 2001): 2002–9. http://dx.doi.org/10.1128/jvi.75.4.2002-2009.2001.

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ABSTRACT In a previous study, we found avian sarcoma and leukosis virus (ASLV) gag genes in 19 species of birds in the order Galliformes including all grouse and ptarmigan (Tetraoninae) surveyed. Our data suggested that retroviruses had been transmitted horizontally among some host species. To further investigate these elements, we sequenced a replication-defective retrovirus, here named tetraonine endogenous retrovirus (TERV), from Bonasa umbellus (ruffed grouse). This is the first report of a complete, replication-defective ASLV provirus sequence from any bird other than the domestic chicken. We found a replication-defective proviral sequence consisting of putative Gag and Env proteins flanked by long terminal repeats. Reverse transcription-PCR analysis showed that retroviral gagsequences closely related to TERV are transcribed, supporting the hypothesis that TERV is an active endogenous retrovirus. Phylogenetic analyses suggest that TERV may have arisen via recombination between different retroviral lineages infecting birds. Southern blotting usinggag probes showed that TERV occurs in tetraonines but not in chickens or ducks, suggesting that integration occurred after the earliest phasianid divergences but prior to the radiation of tetraonine birds.
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Seifarth, Wolfgang, Oliver Frank, Udo Zeilfelder, Birgit Spiess, Alex D. Greenwood, Rüdiger Hehlmann, and Christine Leib-Mösch. "Comprehensive Analysis of Human Endogenous Retrovirus Transcriptional Activity in Human Tissues with a Retrovirus-Specific Microarray." Journal of Virology 79, no. 1 (January 1, 2005): 341–52. http://dx.doi.org/10.1128/jvi.79.1.341-352.2005.

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ABSTRACT Retrovirus-like sequences account for 8 to 9% of the human genome. Among these sequences, about 8,000 pol-containing proviral elements have been identified to date. As part of our ongoing search for active and possibly disease-relevant human endogenous retroviruses (HERVs), we have recently developed an oligonucleotide-based microarray. The assay allows for both the detection and the identification of most known retroviral reverse transcriptase (RT)-related nucleic acids in biological samples. In the present study, we have investigated the transcriptional activity of representative members of 20 HERV families in 19 different normal human tissues. Qualitative evaluation of chip hybridization signals and quantitative analysis by real-time RT-PCR revealed distinct HERV activity in the human tissues under investigation, suggesting that HERV elements are active in human cells in a tissue-specific manner. Most active members of HERV families were found in mRNA prepared from skin, thyroid gland, placenta, and tissues of reproductive organs. In contrast, only few active HERVs were detectable in muscle cells. Human tissues that lack HERV transcription could not be found, confirming that human endogenous retroviruses are permanent components of the human transcriptome. Distinct activity patterns may reflect the characteristics of the regulatory machinery in these cells, e.g., cell type-dependent occurrence of transcriptional regulatory factors.
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Wolgamot, Greg, and A. Dusty Miller. "Replication of Mus dunni Endogenous Retrovirus Depends on Promoter Activation Followed by Enhancer Multimerization." Journal of Virology 73, no. 12 (December 1, 1999): 9803–9. http://dx.doi.org/10.1128/jvi.73.12.9803-9809.1999.

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ABSTRACT Mus dunni endogenous virus (MDEV) is an apparently intact retrovirus that normally lies transcriptionally silent in cultured M. dunni cells, but the provirus can be activated by treatment of the cells with hydrocortisone or 5-iodo-2′-deoxyuridine. Sequence analysis of a molecular clone of the replicating virus revealed a simple retrovirus with a chimeric VL30/GALV-like structure. Interestingly, in the region of the long terminal repeat (LTR) that typically contains the retroviral transcription enhancers, we found over six 80-bp repeats with only a single mismatch, indicating that acquisition of the repeats was a recent event. Here we provide evidence for the following model of MDEV activation and replication. The MDEV provirus in M. dunnicells has a chimeric structure similar to that of the molecular clone but has only 1.15 copies of the 80-bp repeat sequence found in the molecular clone. Activating chemicals directly stimulate transcription from the LTR, allowing a low level of virus replication. Copying errors made during reverse transcription allow multimerization of the 80-bp enhancer region, resulting in viruses with higher transcriptional rates and improved fitness, but increased enhancer copy number is likely balanced by the natural instability of retroviral repeats and constraints imposed by virion packaging limits. The resultant population of replicating MDEV is widely heterogeneous, having from 2.15 to 13.15 enhancer repeats in the LTR. These results reveal a novel mechanism for regulation of transcription and replication of an endogenous retrovirus, in terms of both activation of the virus by the steroid hydrocortisone and the large number and variation in enhancer repeats observed.
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Kogan, Scott C., Mei Lin Maunakea, Karen L. Himmel, Bin Yin, Michelle M. Le Beau, and David A. Largaespada. "Cooperative Pathways to Acute Myeloid Leukemia Include the Combining of Transcription Factor Alterations: PML-RARα Cooperates with SOX4." Blood 104, no. 11 (November 16, 2004): 3385. http://dx.doi.org/10.1182/blood.v104.11.3385.3385.

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Abstract One paradigm for transformation of normal myeloid cells into acute myeloid leukemia (AML) is the combining of transcription factor alteration with activation of signaling pathways, including cytokine receptor activation. To identify possible alternative pathways to leukemogenesis we crossed MRP8-PML/RARA transgenic mice with BXH-2 mice, which harbor an endogenous retrovirus that causes AML. Approximately half of the leukemias that arose in this cross showed features of acute promyelocytic leukemia (APL). We identified 22 insertions sites in 8 APL-like leukemias. Of these, 7 represented common insertion sites in the Mouse Retroviral Tagged Cancer Gene Database (RTCGD, http://rtcgd.ncifcrf.gov/mm4/index.html). We introduced into a retroviral vector cDNAs encoding 6 genes located at retroviral insertion sites identified in PML/RARA leukemias (Sox4, Meis1, Lck, Sfpi1, Nfil3, Cblb). PML/RARA transgenic bone marrow was transduced with these retroviruses and the marrow was used to reconstitute lethally irradiated recipient animals. Recipients of PML/RARα transgenic marrow transduced with a SOX4 retrovirus developed APL-like leukemias in 3 months. SOX4 is an HMG box transcription factor that exhibits sequence specific DNA binding and transactivation. It is the most common insertion site in RTCGD, and has been found to be overexpressed in small cell lung cancer and medulloblastoma, as well as other tumors. In light of other data indicating that combining transcription factor abnormalities can rapidly induce leukemia (e.g. Hoxa9 + Meis1), our finding that SOX4 + PML/RARα is potently leukemogenic supports the hypothesis that such cooperativity represents another important paradigm in myeloid leukemogenesis.
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Pietrantoni, Gianfranco, Rodrigo Ibarra-Karmy, and Gloria Arriagada. "Microtubule Retrograde Motors and Their Role in Retroviral Transport." Viruses 12, no. 4 (April 24, 2020): 483. http://dx.doi.org/10.3390/v12040483.

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Following entry into the host cell, retroviruses generate a dsDNA copy of their genomes via reverse transcription, and this viral DNA is subsequently integrated into the chromosomal DNA of the host cell. Before integration can occur, however, retroviral DNA must be transported to the nucleus as part of a ‘preintegration complex’ (PIC). Transporting the PIC through the crowded environment of the cytoplasm is challenging, and retroviruses have evolved different mechanisms to accomplish this feat. Within a eukaryotic cell, microtubules act as the roads, while the microtubule-associated proteins dynein and kinesin are the vehicles that viruses exploit to achieve retrograde and anterograde trafficking. This review will examine the various mechanisms retroviruses have evolved in order to achieve retrograde trafficking, confirming that each retrovirus has its own strategy to functionally subvert microtubule associated proteins.
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Hansen, Regine, Stefanie Czub, Evi Werder, Jens Herold, Georg Gosztonyi, Hans Gelderblom, Simone Schimmer, Stefan Mazgareanu, Volker ter Meulen, and Markus Czub. "Abundant Defective Viral Particles Budding from Microglia in the Course of Retroviral Spongiform Encephalopathy." Journal of Virology 74, no. 4 (February 15, 2000): 1775–80. http://dx.doi.org/10.1128/jvi.74.4.1775-1780.2000.

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ABSTRACT A pathogenetic hallmark of retroviral neurodegeneration is the affinity of neurovirulent retroviruses for microglia cells, while degenerating neurons are excluded from retroviral infections. Microglia isolated ex vivo from rats peripherally infected with a neurovirulent retrovirus released abundant mature type C virions; however, infectivity associated with microglia was very low. In microglia, viral transcription was unaffected but envelope proteins were insufficiently cleaved into mature viral proteins and were not detected on the microglia cell surface. These microglia-specific defects in envelope protein translocation and processing not only may have prevented formation of infectious virus particles but also may have caused further cellular defects in microglia with the consequence of indirect neuronal damage. It is conceivable that similar events play a role in neuro-AIDS.
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Dissertations / Theses on the topic "Retrovirus transcription"

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BARAT, CORINNE. "Etude de l'initiation de la reserve transcription du genome du retrovirus humain, hiv-1." Paris 6, 1992. http://www.theses.fr/1992PA066024.

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Chez le retrovirus hiv-1, la replication de l'arn genomique viral est assuree par la reserve transcriptase virale rtp66-p51. Cette reserve transcription est initiee a partir d'un trna#l#y#s#,#3 cellulaire hybride a l'arn pres de son extremite 5. Dans une analyse de cette etape d'initiation, nous avons etudie les interactions entre ce trna amorce et les autres membres du complexe d'initiation de la reserve transcription, en particulier la reserve transcriptase rtp66-p51 et la proteine de nucleocapside ncp15. Nous avons montre une interaction specifique entre la reserve transcriptase et le trna#l#y#s#,#3 initiateur, et les sites d'interaction sur le trna et sur la proteine ont pu etre localises. L'importance de la structure en heterodimere de la reverse transcriptase pour son interaction avec le trna amorce et pour son activite polymerase a egalement ete mise en evidence. La proteine de nucleocapside, outre sa capacite a promouvoir la fixation du trna initiateur sur l'arn viral, semble participer a un complexe ternaire avec le trna#l#y#s#,#3 et la reserve transcriptase. Ce complexe pourrait etre implique dans les etapes de selection des trna encapsides, d'hybridation du trna#l#y#s#,#3 a l'arn viral, et d'initiation de la reverse transcription
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Broders, Florence. "Analyse de la transcription des genes alpha globine dans les erythroblastes aviaires normaux et transformes par un retrovirus." Paris 7, 1988. http://www.theses.fr/1988PA077023.

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LAVIGNON, MARC. "Action d'oligonucleotides modifies sur la transcription inverse ou sur la traduction. Etude de leur effet sur la proliferation de retrovirus murins." Paris 7, 1991. http://www.theses.fr/1991PA077241.

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Nous montrons que des oligodesoxyribonucleotides d'anomerie alpha sont capables d'inhiber in vitro l'initiation de la transcription inverse qui est une etape clef du cycle replicatif des retrovirus. En effet, leur hybridation parallele sur une sequence complementaire d'acide nucleique ne leur permet pas de servir d'amorce a la transcriptase inverse. Lors de competitions entre une amorce d'anomerie beta et un oligonucleotide alpha, nous obtenons une inhibition de la synthese d'adn. Par ailleurs, la reconnaissance des duplex alpha-beta par la transcriptase inverse permet de pieger celle-ci et d'inhiber son activite polymerase et rnase h. Ex vivo, nous montrons qu'un oligonucleotide alpha, dirige contre le site de fixation de l'arnt (site pbs) qui sert d'amorce a la transcription inverse chez les retrovirus, est capable de diminuer la dissemination du retrovirus de friend et d'un virus recombinant de moloney. Cette inhibition est observee lors d'une infection de novo de cellules prealablement electropermeabilisees en presence de l'oligonucleotide. Nous emettons l'hypothese que cet oligonucleotide alpha agit lors des etapes tardives de la transcription inverse mettant en jeu le site pbs et non au moment de l'initiation de celle-ci. Enfin, nous montrons que la modification d'un oligodesoxyribonucleotide beta (en l'occurrence l'adjonction d'une molecule de 9-amino-ellipticine en 5), dirige contre le site d'initiation de la synthese de la proteine env, est necessaire pour obtenir un effet sur la proliferation du retrovirus de friend. Ce couplage n'augmente ni l'affinite de l'oligonucleotide pour sa cible ni son activite inhibitrice de la synthese proteique in vitro. Il protege l'oligonucleotide contre les degradations nucleasiques en 3 et facilite, peut etre, sa penetration cellulaire
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Prats, Anne-Catherine. "Etude de l'expression genetique et de la constitution des particules virales infectieuses chez le retrovirus murin mulv." Toulouse 3, 1988. http://www.theses.fr/1988TOU30172.

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Yoshinaga, Noriyoshi. "A screening for DNA damage response molecules that affect HIV-1 infection." Kyoto University, 2019. http://hdl.handle.net/2433/243296.

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Laverdure, Sylvain. "Régulation de la transcription bidirectionnelle chez le Virus de l'Immunodéficience Humaine de type 1." Thesis, Montpellier 1, 2012. http://www.theses.fr/2012MON13514/document.

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Le génome des rétrovirus existe sous deux formes différentes : sous forme d'ARN simple brin, qui est traduit ou encapsidé, ou sous forme d'ADN double brin intégré dans le génome de la cellule hôte infectée. Cette dernière forme, l'ADN proviral, est indispensable à la production de tous les ARNm viraux nécessaires à la synthèse des protéines virales, qui en retour agissent sur la région promotrice située au niveau du LTR 5'. Cependant, l'ADN proviral possède un second LTR à son extrémité 3', capable de réguler une transcription antisens, orientée dans la direction opposée à celle contrôlée par le LTR 5'. L'ADN proviral a donc deux brins codants, ce qui offre au virus un plus grand potentiel de synthèse protéique. Dans le cas du Virus de l'immunodéficience Humaine de type 1 (VIH-1), la transcription antisens permet la production d'une protéine, appelée ASP (Antisense Protein). Dans ce manuscrit, nous démontrons que cette activité transcriptionnelle antisens s'exprime préférentiellement dans les cellules d'origine monocytaire, en particulier les cellules dendritiques ; une localisation membranaire de la protéine ASP a par ailleurs été mise en évidence dans ce type cellulaire. Nos résultats suggèrent également que la transcription antisens du VIH-1 est indépendante de la protéine Tat, et que par ailleurs les deux types de transcriptions ne sont pas exprimés simultanément au sein d'une même cellule. En outre, nos données soulignent que la séquence codante de la protéine ASP est très fortement conservée parmi les différents isolats viraux. Sur la base de l'ensemble de ces résultats, notre hypothèse est que la protéine ASP du VIH-1 possède des fonctions cruciales dans le cycle réplicatif des rétrovirus, indépendantes de la production virale
Genome of retroviruses exists in two different forms: as single-stranded RNA that is translated or packaged, or as double-stranded DNA integrated into the genome of the infected host cell. The latter form, the proviral DNA, is essential for the production of all viral mRNAs required for the synthesis of viral proteins, which in turn act on the promoter region located at the 5 '-LTR. However, the proviral DNA has a second LTR at its 3 '-end, capable of regulating antisense transcription oriented in the opposite direction to that controlled by the 5'-LTR. The proviral DNA has then two coding strands, which gives the virus a greater potential for protein synthesis. In the case of the Human Immunodeficiency Virus type 1 (HIV-1), antisense transcription allows the production of a protein called ASP (Antisense Protein). In this manuscript, we demonstrate that this antisense transcriptional activity is preferentially expressed in cells of the monocyte lineage, in particular dendritic cells; a membrane localization of the ASP protein was also observed in this cell type. Our results also suggest that the antisense transcription of HIV-1 is Tat-independent, and what's more that the two types of transcription are not expressed simultaneously within the same cell. In addition, our data highlight that the ASP protein coding sequence is highly conserved among different viral isolates. Based on these results, our hypothesis is that the ASP protein of HIV-1 has critical functions in the replicative cycle of retroviruses, distinct from viral production
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ROUSSET, RAPHAEL. "Caracterisation des interactions entre l'oncoproteine tax1 du retrovirus htlv-i et differents facteurs cellulaires impliques dans le controle de la transcription et de la proliferation." Lyon, École normale supérieure (sciences), 1997. http://www.theses.fr/1997ENSL0069.

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L'infection par le retrovirus htlv-i entraine divers syndromes proliferatifs et degeneratifs chez l'homme. La proteine tax1, produite par le virus, possede des activites transactivatrices et oncogeniques qui sont en grande partie responsables des pathologies associees a htlv-i. Les etudes que nous avons engagees ont permis de caracteriser plusieurs proteines qui interagissent avec tax1 dans la cellule. Des etudes effectuees in vivo et in vitro montrent que tax1 favorise la premiere etape de la mise en place du complexe d'initiation de la transcription, en recrutant directement tfiid. Par ailleurs, le systeme du simple hybride dans la levure a permis d'identifier 3 facteurs de transcription, creb, crem et atf1, capables de cooperer in vivo avec tax1 sur le motif tre1 du promoteur htlv-i. Dans un deuxieme temps, nous avons recherche d'autres partenaires cellulaires de tax1 par un criblage avec le systeme des deux hybrides dans la levure. Deux sous-unites du proteasome, hc9 et hsn3, ont ete ainsi isolees. Une etude fonctionnelle suggere que tax1 favorise l'association de p105 avec le proteasome et accelere ainsi le clivage de p105 en p50 dans la voie nf-b. Lors de ce criblage, nous avons egalement isole l'homologue humain de la proteine de souris int-6 impliquee dans la proliferation cellulaire. En interagissant avec hint-6, tax1 altere sa localisation nucleaire en points. Ce mecanisme pourrait modifier la fonction d'hint-6 et donc participer au processus de transformation cellulaire induit par tax1. Enfin, six nouvelles proteines contenant des domaines pdz ont ete isolees. Leur interaction avec tax1 est assuree par l'extremite c-terminale de la proteine virale, qui possede le motif consensus x-t/s-x-v-cooh implique dans l'interaction avec les domaines pdz. De part les fonctions des proteines de cette famille dans la cellule, il est possible que ces interactions soient a l'origine de certains desordres proliferatifs et degeneratifs qui sont associes a htlv-i.
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Hu, Lijuan. "Endogenous Retroviral RNA Expression in Humans." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Universitetsbiblioteket [distributör], 2007. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8213.

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TOUNEKTI, NACEUR. "Etude structurale de l'extremite cinq prime terminale non codante de l'arn du retrovirus murin de moloney : application a l'etude de la dimerisation et du complexe d'initiation de la transcription inverse." Paris 11, 1993. http://www.theses.fr/1993PA112452.

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Dans le but d'inhiber la propagation retrovirale par des oligonucleotides de synthese nous avons mene une etude physico-chimique et structurale des phenomenes de dimerisation et de formation du complexe d'initiation de la transcription inverse. Nous avons montre que la dimerisation de l'arn du virus de moloney (mo-mulv) est un processus lent qui implique d'une part, des changements structuraux au sein de la sequence d'encapsidation psi (particulierement les sequences: deux cent dix-deux cent vingt) et (deux cent soixante dix-huit-trois cent dix) et d'autre part, des transitions conformationnelles au niveau des regions adjacentes a psi. Nous avons aussi montre que psi garde une structure intrinseque independante du reste de la molecule d'arn. Par ailleurs, la formation du complexe d'initiation de la transcription inverse, par fixation specifique de l'arn#t proline sur le site pbs, induit des changements structuraux au sein de la sequence (un-deux cent quinze) et impliquerait d'autres interactions entre l'amorce et l'arn viral. Enfin le ciblage du site pbs ou de sequences particulieres au sein de psi par des oligonucleotides de synthese a abouti a une inhibition significative de la replication retrovirale
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Mommert, Marine. "Modulation de l'expression des rétrovirus endogènes humains dans des contextes d'inflammation et d'immunosuppression." Thesis, Lyon, 2018. http://www.theses.fr/2018LYSEN044.

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Le sepsis est défini par l’apparition de dysfonctions d’organes, multiples et mortelles, causées par une réponse de l’hôte dérégulée suite à une infection. L’hétérogénéité de la maladie représente un défi clinique majeur au regard de la prise en charge thérapeutique, et à ce jour les marqueurs proposés ne suffisent pas à stratifier les patients. Les rétrovirus endogènes humains (HERV) pourraient être des marqueurs pertinents,compte tenu des propriétés immunosuppressives de leurs enveloppes et de leur expression dans des maladies inflammatoires et auto-immunes. Cette thèse a pour objectif de savoir dans quelle mesure les HERV sont exprimés et modulés, dans des conditions d’inflammation et d’immunosuppression. Pour cela,nous avons utilisé une puce à ADN haute densité permettant (i) l’analyse de la transcription de 363 689HERV et 1500 gènes, et (ii) une lecture fonctionnelle de l’activité des LTR. L’expression des HERV a été objectivée (i) dans un modèle ex-vivo de tolérance à l’endotoxine sur des cellules mononuclées du sang périphérique (PBMC) d’individus sains et (ii) sur sang total provenant d’individus sains et de patients en choc septique, stratifiés ou non en fonction du statut immunitaire. (1) De 5,6% à 6,9% des HERV sont exprimés dans le compartiment sanguin et environ 20% des LTR possèdent une fonction promotrice ou polyA, les deux fonctions étant mutuellement exclusives. (2) Le contenu du transcriptome HERV est modulé ex vivo dans le contexte de tolérance à l’endotoxine laissant apparaitre deux grands phénotypes transcriptionnels. L’expression de certains loci HERV est corrélée au statut immunitaire de patient septique.L’évaluation d’une signature moléculaire complexe sur une cohorte de validation, permet la séparation en deux groupes présentant des critères de sévérité distincts, suggérant les HERV/MaLR comme biomarqueurs de stratification. (3) L’analyse de la co-expression des gènes et des HERV a permis d’intégrer ceux-ci au sein de réseaux associées à la réponse de l’hôte et de proposer des hypothèses fonctionnelles
Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection.The heterogeneity of the disease present a major clinical challenge with regard to the therapeutic coverage,and this day the proposed markers are not enough to stratify patients. The human endogenous retrovirus(HERV) could be relevant markers, considering the immunosuppressives properties of their envelopes andtheir expression in inflammatory and autoimmune disease. The aim of this thesis is to know to what extentthe HERVs are expressed and modulated, in inflammatory and immunocompromised contexts. For this, weused a high density DNA chip allowing (i) the transcription analysis of 363,689 HERV and 1500 genes,and (ii) a functional reading of LTRs activities. The HERVs expression was objectified (i) in endotoxintolerance ex vivo model in peripheral blood mononuclear cells (PBMCs) of healthy volunteers and (ii) inwhole blood of healthy volunteers and septic shock patients, stratified or not according to immunity state.(1) Of 5,6% at 6,9% of HERVs are expressed in the blood compartment and around 20% of LTRs have apromoter or polyA function, both functions being mutually exclusive. (2) The HERV transcriptome ismodulated in ex vivo endotoxin tolerance model letting appear two higher transcriptional phenotypes. Theexpression of some HERVs loci are correlated of the immunity state of the septic shock patients. Theevaluation of molecular signature in validation cohort, allowed to separate in two patients groupspresenting different severity criteria, suggesting HERV/MaLR as biomarkers of stratification. (3) The coexpressedanalysis of genes and HERVs allowed to integrate these within signaling pathways associated atthe host immune response and to provide functional hypothesis
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Books on the topic "Retrovirus transcription"

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Kim, Hŭi-su. Tayang han twaeji PERV ŭi t'ŭksŏng kyumyŏng mit Han'gugin sep'oju rŭl iyong han LTR ŭi chŏnsa chojŏl kijak kyumyŏng =: Characterization of various pig PERV element and transcription regulation mechanism of LTR elements in Korean cell lines. [Kyŏnggi-do Suwŏn-si]: Nongch'on Chinhŭngch'ŏng, 2009.

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1957-, Pomerantz Roger J., ed. Retroviral latency. Austin: R.G. Landes, 1994.

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Retroviruses: Molecular biology, genomics and pathogenesis. Norfolk, UK: Caister Academic, 2010.

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

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1938-, Yaniv Moshe, and Ghysdael J, eds. Oncogenes as transcriptional regulators. Basel: Birkhäuser Verlag, 1997.

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International Conference on Gene Regulation, Oncogenesis, and AIDS (1st 1989 Loutráki, Greece). Gene regulation and AIDS: Transcriptional activation, retroviruses, and pathogenesis : papers delivered at the First International Conference on Gene Regulation, Oncogenesis, and AIDS, Loutráki, Greece, September 15-21, 1989. Edited by Papas Takis S. Woodlands, Texas: Portfolio Pub. Co., 1990.

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Chen, Irvin S. Y. Transacting Functions Of Human Retroviruses (Current Topics in Microbiology & Immunology). Edited by Irvin S. Y. Chen. Springer, 1995.

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LITVAK, SIMON. Retroviral Reverse Transcriptases. Chapman & Hall, 1996.

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(Editor), M. Yaniv, and J. Ghysdael (Editor), eds. Oncogenes as Transcriptional Regulators: Volume 1: Retroviral Oncogenes (Progress in Gene Expression). Birkhauser, 1997.

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Papas, Takis S. Gene Regulation And AIDS: Transcriptional Activation, Retroviruses, and Pathogenesis (Advances in Applied Biotechnology Series, Vol 7). Gulf Pub Co, 1990.

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Book chapters on the topic "Retrovirus transcription"

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Chen, P. J., A. Cywinski, and J. M. Taylor. "Participation of 7S L RNA in Reverse Transcription by an Avian Retrovirus." In International Symposium: Retroviruses and Human Pathology, 227–34. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-5008-1_19.

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Panganiban, Antonito. "Strand Switching During Retroviral Reverse Transcription." In Vectors as Tools for the Study of Normal and Abnormal Growth and Differentiation, 113–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-642-74197-5_10.

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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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Hughes, Stephen H. "Reverse Transcription of Retroviruses and LTR Retrotransposons." In Mobile DNA III, 1051–77. Washington, DC, USA: ASM Press, 2015. http://dx.doi.org/10.1128/9781555819217.ch46.

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Kjeldgaard, Niels Ole, Allan J. Bækgaard, Hong Yan Dai, Michael Etzerodt, Poul Jørgensen, Steen Lovmand, Henrik Steen Olsen, and Finn Skou Pedersen. "Transcriptional Control by Retroviral LTR Regions." In Evolutionary Tinkering in Gene Expression, 87–99. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5664-6_9.

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Jabeen, Rukhsana. "Retroviral Transduction and Reporter Assay: Transcription Factor Cooperation in Th9 Cell Development." In Methods in Molecular Biology, 155–66. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6877-0_12.

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Sugden, Bill. "Reprint of Temin's 1993 Paper on the Inherent Contributions of Reverse Transcription to Retroviral Variation." In The DNA Provirus, 215–20. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555818302.ch15.

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Toledano, Michel, and Allen J. Aksamit Jr. "Retroviral Infections of the Nervous System." In Mayo Clinic Neurology Board Review, edited by Kelly D. Flemming, 1009–15. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197512166.003.0112.

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Retroviruses are a family of RNA viruses that replicate by reverse transcription. The family includes HIV and human T-lymphotropic virus. This chapter reviews neurologic manifestations of these retroviruses. A retrovirus in the genus Lentivirus, HIV has 2 forms, HIV-1 and HIV-2. HIV-1 is associated with the global AIDS pandemic, whereas HIV-2 causes an AIDS-like illness primarily in West Africa, although pockets of infection exist globally.
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Goff, Stephen P. "Cellular Factors That Regulate Retrovirus Uncoating and Reverse Transcription." In Retrovirus-Cell Interactions, 51–112. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-811185-7.00002-9.

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Leis, Jonathan, and Ashok Aiyar. "[16] Retrovirus reverse transcription and integration." In Viral Gene Techniques, 254–66. Elsevier, 1995. http://dx.doi.org/10.1016/s1067-2389(06)80048-8.

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Conference papers on the topic "Retrovirus transcription"

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Agoni, Lorenzo, Jack Lenz, and Chandan Guha. "Abstract 4346: Influence of ionizing radiation on transcription of human endogenous retrovirus-K (HERV-K) in breast cancer cell lines." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-4346.

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Reports on the topic "Retrovirus transcription"

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Davidson, Irit, Hsing-Jien Kung, and Richard L. Witter. Molecular Interactions between Herpes and Retroviruses in Dually Infected Chickens and Turkeys. United States Department of Agriculture, January 2002. http://dx.doi.org/10.32747/2002.7575275.bard.

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Tumors in commercial poultry are caused mainly by infection with avian herpes and retroviruses, the herpesvirus Marek's disease virus (MDV) and the retroviruses, reticuloendotheliosis (REV), lymphoid leukosis, subgroups A-I and J (ALV and ALV-J) in chickens, or Iymphoprolipherative disease (LPDV) in turkeys. Infection with one virus aggravates the clinical outcome of birds that are already infected by another oncogenic virus. As these viruses do not interfere for infection, MDV and one or more retroviruses can infect the same flock, the same bird and the same cell. While infecting the same cell, herpes and retroviruses might interact in at least three ways: a) Integration of retrovirus genomes, or genomic fragments (mainly the LTR) into MDV;b) alteration of LTR-driven expression of retroviral genes by MDV immediate- early genes, and c) by herpesvirus induced cellular transcriptional factors. The first type of molecular interaction have been demonstrated to happen efficiently in vitro by Dr. Kung, in cases multiple infection of cell cultures with MDV and REV or MDV and ALV. Moreover, Dr. Witter showed that an in vitro-created recombinant, RM1, had altered in vitro replication and in vivo biological properties. A more comprehensive characterization of RM1 was carried out in the present project. We sought to highlight whether events of such integrations occur also in the bird, in vivo. For that, we had first to determine the prevalence of dually-infected individual birds in commercial flocks, as no systematic survey has been yet reported. Surprisingly, about 25% of the commercial flocks infected with avian oncogenic viruses had a multiple virus infection and 5% of the total samples ana lysed had multiple virus sequences. Then, we aimed to evaluate and characterize biologically and molecularly the resulting recombinants, if formed, and to analyse the factors that affect these events (virus strains, type and age of birds and time interval between the infection with both viruses). The perception of retrovirus insertions into herpesviruses in vivo is not banal, as the in vivo and in vitro systems differ in the viral-target cells, lymphocytes or fibroblasts, in the MDV-replicative type, transforming or productive, and the immune system presence. We realized that previous methods employed to study in vitro created recombinant viruses were not adequate for the study of samples taken directly from the bird. Therefore, the Hot Spot-combined PCR was developed based on the molecularly known RM1 virus. Also, the PFGE that was used for tissue cultured-MDV separation was inefficient for separating MDV from organs, but useful with feather tips as a source of bird original MDV. Much attention was dedicated now to feathers, because if a recombinant virus would be formed in vivo, its biological significance would be evident by horizontal dissemination through the feathers. Major findings were: a) not only in vitro, but also in vivo MDV and retrovirus co-infections lead to LTR integrations into MDV. That was shown by the detection of chimeric molecules. These appeared in low quantities and as quasispecies, thus interfering with sequence analysis of cloned gel-purified chimeric molecules. Mainly inserts were located in the repeat long MDV fragments. In field birds chimeric molecules were detected at a lower frequency (2.5%) than in experimentally infected birds (30-50%). These could be transmitted experimentally to another birds by inoculation with chimeric molecules containing blood. Several types of chimeric molecules were formed, and same types were detected in birds infected by a second round. To reproduce viral integrations, in vivo infection trials were done with field inoculate that contained both viruses, but the chimeric molecule yield was undetectable.
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