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Relevant bibliographies by topics / Retroviral replication cycle

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Journal articles
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Academic literature on the topic 'Retroviral replication cycle'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Retroviral replication cycle"

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BORIS-LAWRIE, KATHLEEN, and HOWARD M. TEMIN. "The Retroviral Vector: Replication Cycle and Safety Considerations for Retrovirus-Mediated Gene Therapy." Annals of the New York Academy of Sciences 716, no. 1 Gene Therapy (1994): 59–71. http://dx.doi.org/10.1111/j.1749-6632.1994.tb21703.x.

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Zhang, Jiayou. "Host RNA polymerase II makes minimal contributions to retroviral frame-shift mutations." Journal of General Virology 85, no. 8 (2004): 2389–95. http://dx.doi.org/10.1099/vir.0.80081-0.

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The rate of mutation during retrovirus replication is high. Mutations can occur during transcription of the viral genomic RNA from the integrated provirus or during reverse transcription from viral RNA to form viral DNA or during replication of the proviral DNA as the host cell is dividing. Therefore, three polymerases may all contribute to retroviral evolution: host RNA polymerase II, viral reverse transcriptases and host DNA polymerases, respectively. Since the rate of mutation for host DNA polymerase is very low, mutations are more likely to be caused by the host RNA polymerase II and/or th

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Lehmann-Che, Jacqueline, Marie-Lou Giron, Olivier Delelis, et al. "Protease-Dependent Uncoating of a Complex Retrovirus." Journal of Virology 79, no. 14 (2005): 9244–53. http://dx.doi.org/10.1128/jvi.79.14.9244-9253.2005.

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ABSTRACT Although retrovirus egress and budding have been partly unraveled, little is known about early stages of the replication cycle. In particular, retroviral uncoating, a process during which incoming retroviral cores are altered to allow the integration of the viral genome into host chromosomes, is poorly understood. To get insights into these early events of the retroviral cycle, we have used foamy complex retroviruses as a model. In this report, we show that a protease-defective foamy retrovirus is noninfectious, although it is still able to bud and enter target cells efficiently. Simi

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Wainberg, Mark A., Andre Dascal, and Jack Mendelson. "Anti-Retroviral Strategies for AIDS and Related Diseases." Canadian Journal of Infectious Diseases 2, no. 3 (1991): 121–28. http://dx.doi.org/10.1155/1991/487657.

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The replication cycle of human immunodeficiency virus type 1 (HIV-1) and other retroviruses consists of four stages: attachment of the virus to specific receptors on the cell surface; uncoating of the viral nucleic acid and conversion to DNA; production of viral RNA and proteins; and assembly and liberation of progeny virus from the cell. Each of these steps represents a potential target for antiviral chemotherapy. Combinations of drugs which act against different steps in the viral replication cycle might be expected to have synergistic potential. Zidovudine (AZT) is the most widely used drug

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Katz, Richard A., James G. Greger, and Anna Marie Skalka. "Effects of cell cycle status on early events in retroviral replication." Journal of Cellular Biochemistry 94, no. 5 (2005): 880–89. http://dx.doi.org/10.1002/jcb.20358.

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Li, Ting, and Jiayou Zhang. "Intramolecular Recombinations of Moloney Murine Leukemia Virus Occur during Minus-Strand DNA Synthesis." Journal of Virology 76, no. 19 (2002): 9614–23. http://dx.doi.org/10.1128/jvi.76.19.9614-9623.2002.

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ABSTRACT Retroviral recombination can occur between two viral RNA molecules (intermolecular) or between two sequences within the same RNA molecule (intramolecular). The rate of retroviral intramolecular recombination is high. Previous studies showed that, after a single round of replication, 50 to 60% of retroviral recombinations occur between two identical sequences within a Moloney murine leukemia virus-based vector. Recombination can occur at any polymerization step within the retroviral replication cycle. Although reverse transcriptase is assumed to contribute to the template switches, pre

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Shin, Nam-Hee, Dennis Hartigan-O'Connor, Julie K. Pfeiffer, and Alice Telesnitsky. "Replication of Lengthened Moloney Murine Leukemia Virus Genomes Is Impaired at Multiple Stages." Journal of Virology 74, no. 6 (2000): 2694–702. http://dx.doi.org/10.1128/jvi.74.6.2694-2702.2000.

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ABSTRACT It has been assumed that RNA packaging constraints limit the size of retroviral genomes. This notion of a retroviral “headful” was tested by examining the ability of Moloney murine leukemia virus genomes lengthened by 4, 8, or 11 kb to participate in a single replication cycle. Overall, replication of these lengthened genomes was 5- to 10-fold less efficient than that of native-length genomes. When RNA expression and virion formation, RNA packaging, and early stages of replication were compared, long genomes were found to complete each step less efficiently than did normal-length geno

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Masson, Christel, Stéphanie Bury-Moné, Elvire Guiot, et al. "Ku80 Participates in the Targeting of Retroviral Transgenes to the Chromatin of CHO Cells." Journal of Virology 81, no. 15 (2007): 7924–32. http://dx.doi.org/10.1128/jvi.02015-06.

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ABSTRACT The heterodimer Ku70/80 Ku is the DNA-binding component of the DNA-PK complex required for the nonhomologous end-joining pathway. It participates in numerous nuclear processes, including telomere and chromatin structure maintenance, replication, and transcription. Ku interacts with retroviral preintegration complexes and is thought to interfere with the retroviral replication cycle, in particular the formation of 2-long terminal repeat (LTR) viral DNA circles, viral DNA integration, and transcription. We describe here the effect of Ku80 on both provirus integration and the resulting t

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Zhang, J., and H. Temin. "Rate and mechanism of nonhomologous recombination during a single cycle of retroviral replication." Science 259, no. 5092 (1993): 234–38. http://dx.doi.org/10.1126/science.8421784.

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DeHart, Jason L., Joshua L. Andersen, Erik S. Zimmerman, et al. "The Ataxia Telangiectasia-Mutated and Rad3-Related Protein Is Dispensable for Retroviral Integration." Journal of Virology 79, no. 3 (2005): 1389–96. http://dx.doi.org/10.1128/jvi.79.3.1389-1396.2005.

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ABSTRACT Integration into the host cell DNA is an essential part of the retroviral life cycle and is required for the productive replication of a retrovirus. Retroviral integration involves cleavage of the host DNA and insertion of the viral DNA, forming an integration intermediate that contains two gaps, each with a viral 5′ flap. The flaps are then removed, and the gap is filled by as yet unidentified nuclease and polymerase activities. It is thought that repair of these gaps flanking the site of retroviral integration is achieved by host DNA repair machinery. The ATM and Rad3-related protei

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Dissertations / Theses on the topic "Retroviral replication cycle"

1

Bhella, David. "The three-dimensional structure of TY1 retrotransposon virus-like particles." Thesis, Birkbeck (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.314149.

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Inacio, Mamede Joao Filipe. "Interactions de la capside de lentivirus de primates avec les facteurs cellulaires de l’hôte." Thesis, Montpellier 1, 2012. http://www.theses.fr/2012MON13524/document.

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Depuis la découverte du virus de l'Immunodéficience humaine, un lentivirus, comme agent pathogène responsable de l'épidémie du SIDA en 1983, beaucoup de progrès sur le sujet ont été réalisés. Il existe deux types de virus différents pouvant infecter l'Homme, le HIV-1 et le HIV-2. Ces deux virus se regroupent en différents groupes et sous-types qui témoignent d'une grande diversité inter et intra individus (notions de quasi-espèces). La découverte de lentivirus infectant naturellement au moins quarante-cinq espèces de primates en Afrique sub-saharienne, a permis un enrichissement des connaissan

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Beckham, Carla Jolene. "Analysis of Connections Between Host Cytoplasmic Processing Bodies and Viral Life Cycles." Diss., The University of Arizona, 2007. http://hdl.handle.net/10150/194209.

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In the past few years, cytoplasmic processing bodies (P-Bodies) have been identified in eukaryotic cells. P-bodies have roles in translational repression, mRNA storage, mRNA decay and are conserved cytoplasmic aggregations of non-translating mRNAs in conjunction with translation repression and mRNA degradation factors. In this work, I, in collaboration with others provide evidence for a new biological role for P-bodies in viral life cycles. This work can be summarized thus:In a collaborative effort, I have identified connections between retrovirallike transposon life cycles and P-bodies. For e

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Blot, Vincent. "Trafic intracellulaire des protéines de structure retrovirales au cours des étapes tardives du cycle replicatif." Paris 7, 2003. http://www.theses.fr/2003PA077203.

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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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Štafl, Kryštof. "Molekulární mechanismy buněčné nepermisivity vůči viru Rousova sarkomu." Master's thesis, 2017. http://www.nusl.cz/ntk/nusl-355717.

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Most viruses can infect only a reduced range of organisms and an effective replication is possible only in selected hosts. These hosts are called permissive for the virus. Molecular principles of a nonpermissiveness and viral mechanisms of overcoming replication obstacles are still not clearly elucidated. This thesis discusses the molecular causes of the cellular nonpermissiveness against a model retrovirus - Rous sarcoma virus. The research is conducted on duck cells which are semipermis- sive to the subgroup C of Rous sarcoma virus. The virus can enter those cells, but it is not able to prod

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