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Relevant bibliographies by topics / Moloney murine leukemia virus; Therapy

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Academic literature on the topic 'Moloney murine leukemia virus; Therapy'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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Journal articles on the topic "Moloney murine leukemia virus; Therapy"

1

Rothenberg, S. Michael, Mari N. Olsen, Louise Chang Laurent, Rachel Adams Crowley, and Patrick O. Brown. "Comprehensive Mutational Analysis of the Moloney Murine Leukemia Virus Envelope Protein." Journal of Virology 75, no. 23 (December 1, 2001): 11851–62. http://dx.doi.org/10.1128/jvi.75.23.11851-11862.2001.

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ABSTRACT The envelope (Env) protein of Moloney murine leukemia virus is the primary mediator of viral entry. We constructed a large pool of insertion mutations in the env gene and analyzed the fitness of each mutant in completing two critical steps in the virus life cycle: (i) the expression and delivery of the Env protein to the cell surface during virion assembly and (ii) the infectivity of virions displaying the mutant proteins. The majority of the mutants were poorly expressed at the producer cell surface, suggesting folding defects due to the presence of the inserted residues. The mutants with residual infectivity had insertions either in the amino-terminal signal sequence region, two disulfide-bonded loops in the receptor binding domain, discrete regions of the carboxy-terminal region of the surface subunit (SU), or the cytoplasmic tail. Insertions that allowed the mutants to reach the cell surface but not to mediate detectable infection were located within the amino-terminal sequence of the mature Env, within the SU carboxy-terminal region, near putative receptor binding residues, and throughout the fusion peptide. Independent analysis of select mutants in this group allowed more precise identification of the defect in Env function. Mapping of mutant phenotypes to a structural model of the receptor-binding domain provides insights into the protein's functional organization. The high-resolution functional map reported here will be valuable for the engineering of the Env protein for a variety of uses, including gene therapy.

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Diaz, R. M., T. Eisen, I. R. Hart, and R. G. Vile. "Exchange of Viral Promoter/Enhancer Elements with Heterologous Regulatory Sequences Generates Targeted Hybrid Long Terminal Repeat Vectors for Gene Therapy of Melanoma." Journal of Virology 72, no. 1 (January 1, 1998): 789–95. http://dx.doi.org/10.1128/jvi.72.1.789-795.1998.

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ABSTRACT To generate transcriptionally targeted vectors, tissue-specific elements of the human tyrosinase promoter were exchanged with corresponding viral elements in the Moloney murine leukemia virus long terminal repeat (LTR). From these experiments, a vesicular stomatitis virus type G pseudotyped, hybrid LTR vector that contained three tyrosinase enhancer elements and gave high-level, tightly tissue-specific expression at high titers (3 × 107CFU/ml) was constructed.

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Hock, RA, AD Miller, and WR Osborne. "Expression of human adenosine deaminase from various strong promoters after gene transfer into human hematopoietic cell lines." Blood 74, no. 2 (August 1, 1989): 876–81. http://dx.doi.org/10.1182/blood.v74.2.876.876.

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Abstract Adenosine deaminase (ADA) deficiency is associated with a fatal severe combined immunodeficiency. Because most patients do not have a suitable marrow donor, the introduction of a normal ADA gene into the patient's marrow cells is a potentially useful alternative therapy. To identify vectors that provide optimal gene expression in human hematopoietic cells, we investigated retroviral vectors containing the ADA gene under the transcriptional control of the promoter/enhancers of Moloney murine leukemia virus, the simian virus 40 early region, the cytomegalovirus immediate-early gene, the lymphotropic papovavirus, and the human beta- globin gene. ADA expression from these vectors was monitored in the ADA- human histiocytic lymphoma cell line DHL-9, and in the multipotential chronic myeloid leukemia cell line K562. ADA expression in infected K562 cells was also measured after induction of megakaryoblastic differentiation by phorbol ester, and after induction of erythroid differentiation by sodium n-butyrate or hemin. In these hematopoietic cell lines, the vectors that contained ADA controlled by either the Moloney murine leukemia virus promoter (LASN) or the cytomegalovirus promoter (LNCA) expressed ADA at much higher levels than the other vectors tested. Furthermore, in K562 cells infected with LASN and LNCA vectors, induction of terminal differentiation resulted in the same or higher level expression of ADA. These cell lines have permitted the evaluation of transduced gene expression in proliferating and differentiating hematopoietic cells that provide a model for bone marrow-targeted gene therapy.

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Hock, RA, AD Miller, and WR Osborne. "Expression of human adenosine deaminase from various strong promoters after gene transfer into human hematopoietic cell lines." Blood 74, no. 2 (August 1, 1989): 876–81. http://dx.doi.org/10.1182/blood.v74.2.876.bloodjournal742876.

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Adenosine deaminase (ADA) deficiency is associated with a fatal severe combined immunodeficiency. Because most patients do not have a suitable marrow donor, the introduction of a normal ADA gene into the patient's marrow cells is a potentially useful alternative therapy. To identify vectors that provide optimal gene expression in human hematopoietic cells, we investigated retroviral vectors containing the ADA gene under the transcriptional control of the promoter/enhancers of Moloney murine leukemia virus, the simian virus 40 early region, the cytomegalovirus immediate-early gene, the lymphotropic papovavirus, and the human beta- globin gene. ADA expression from these vectors was monitored in the ADA- human histiocytic lymphoma cell line DHL-9, and in the multipotential chronic myeloid leukemia cell line K562. ADA expression in infected K562 cells was also measured after induction of megakaryoblastic differentiation by phorbol ester, and after induction of erythroid differentiation by sodium n-butyrate or hemin. In these hematopoietic cell lines, the vectors that contained ADA controlled by either the Moloney murine leukemia virus promoter (LASN) or the cytomegalovirus promoter (LNCA) expressed ADA at much higher levels than the other vectors tested. Furthermore, in K562 cells infected with LASN and LNCA vectors, induction of terminal differentiation resulted in the same or higher level expression of ADA. These cell lines have permitted the evaluation of transduced gene expression in proliferating and differentiating hematopoietic cells that provide a model for bone marrow-targeted gene therapy.

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Seamon, Jennifer A., Kathryn S. Jones, Christina Miller, and Monica J. Roth. "Inserting a Nuclear Targeting Signal into a Replication-Competent Moloney Murine Leukemia Virus Affects Viral Export and Is Not Sufficient for Cell Cycle-Independent Infection." Journal of Virology 76, no. 16 (August 15, 2002): 8475–84. http://dx.doi.org/10.1128/jvi.76.16.8475-8484.2002.

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ABSTRACT The effects of inserting reported nuclear localization signals (NLSs) into the Moloney murine leukemia virus (Mo-MuLV) integrase (IN) protein, within a replication-competent viral construct, were studied. In contrast to the virus harboring IN fused to the simian virus 40 (SV40) large T antigen NLS (SV40 NLS) (J. A. Seamon, M. Adams, S. Sengupta, and M. J. Roth, Virology 274:412-419, 2000), a codon-modified SV40 NLS was stably expressed during viral propagation. Incorporation of the codon-modified SV40 NLS into IN, however, altered the packaging of the Gag-Pol precursor in the virus; viral particles contained decreased levels of reverse transcriptase (RT) and IN. In addition, the virus showed delayed kinetics of viral DNA synthesis upon infection. A panel of infectious MuLVs containing alternative IN-NLS fusions was generated and assayed for cell cycle-independent infection. Viral infection with the NLS-tagged proteins, however, remained dependent on passage of the cells through mitosis. This finding has direct implications for engineering murine-based retroviral vectors for gene therapy.

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Eckert, HG, M. Stockschlader, U. Just, S. Hegewisch-Becker, M. Grez, A. Uhde, A. Zander, W. Ostertag, and C. Baum. "High-dose multidrug resistance in primary human hematopoietic progenitor cells transduced with optimized retroviral vectors." Blood 88, no. 9 (November 1, 1996): 3407–15. http://dx.doi.org/10.1182/blood.v88.9.3407.bloodjournal8893407.

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Retroviral transfer of the multidrug-resistance 1 (mdr1) cDNA into primary human hematopoietic progenitor cells (HPC) of cancer patients undergoing high-dose chemotherapy has been proposed to protect the bone marrow from the dose-limiting cytotoxicity of cytostatic agents. Preclinical studies performed with vectors derived from the Moloney murine leukemia virus (MoMuLV) or the related Harvey murine sarcoma virus have established that chemoprotection of HPC is feasible. The efficacy of vector-mediated multidrug-resistance under high doses of cytostatic agents, however, remained unclear. We report here that this goal can only be achieved with improved vector design. Novel vectors termed SF-MDR and MP-MDR, which are based on the spleen focus-forming virus or the myeloproliferative sarcoma virus for the enhancer and the murine embryonic stem cell virus for the leader, significantly elevate survival of transduced primary human HPC under moderate doses of colchicine and paclitaxel in vitro when compared with a conventional MoMuLV-based vector. Importantly, SF-MDR and also MP-MDR confer an absolute advantage at high doses of paclitaxel in vitro corresponding to peak plasma levels achieved in patients during chemotherapy. This observation has important consequences for a variety of ongoing and planned gene therapy trials.

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Sharkey, C. Matthew, Cynthia L. North, Richard J. Kuhn, and David Avram Sanders. "Ross River Virus Glycoprotein-Pseudotyped Retroviruses and Stable Cell Lines for Their Production." Journal of Virology 75, no. 6 (March 15, 2001): 2653–59. http://dx.doi.org/10.1128/jvi.75.6.2653-2659.2001.

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ABSTRACT Pseudotyped retroviruses have important applications as vectors for gene transfer and gene therapy and as tools for the study of viral glycoprotein function. Recombinant Moloney murine leukemia virus (Mo-MuLV)-based retrovirus particles efficiently incorporate the glycoproteins of the alphavirus Ross River virus (RRV) and utilize them for entry into cells. Stable cell lines that produce the RRV glycoprotein-pseudotyped retroviruses for prolonged periods of time have been constructed. The pseudotyped viruses have a broadened host range, can be concentrated to high titer, and mediate stable transduction of genes into cells. The RRV glycoprotein-pseudotyped retroviruses and the cells that produce them have been employed to demonstrate that RRV glycoprotein-mediated viral entry occurs through endocytosis and that membrane fusion requires acidic pH. Alphavirus glycoprotein-pseudotyped retroviruses have significant advantages as reagents for the study of the biochemistry and prevention of alphavirus entry and as preferred vectors for stable gene transfer and gene therapy protocols.

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Viejo-Borbolla, A., P. Thomas, E. D. Blair, and T. F. Schulz. "Increase in infectivity of targeted Moloney murine leukemia virus-based gene-delivery vectors through lowering the threshold for fusion." Journal of General Virology 86, no. 9 (September 1, 2005): 2469–80. http://dx.doi.org/10.1099/vir.0.81057-0.

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Many research groups have developed targeted vectors for gene therapy based on Moloney murine leukemia virus (MoMLV). Despite proper binding of the targeted vector to the target molecule, little or no infectivity of human cells expressing the target molecule has been achieved in most studies. One of the reasons for this lack of infectivity may be steric hindrance within the targeted envelope glycoprotein (Env), impeding the conformational changes required for fusion and infection. Here, attempts were made to solve this problem by mutating key residues within Env of two targeted MoMLV-based vectors, MoMLV–E-Sel and MoMLV–FBP. Selection of key residues was based on an Env with reduced threshold for fusion, that of the CD4-independent human immunodeficiency virus type 2 isolate ROD/B. It was shown here that vectors bearing MoMLV–FBP Env with a V512M substitution had higher titres and faster kinetics of entry than vectors bearing parental targeted Env proteins. This could be due to the partial release of steric constraints that result in an Env with a reduced threshold for fusion.

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van Beusechem, V. W., A. Kukler, M. P. Einerhand, T. A. Bakx, A. J. van der Eb, D. W. van Bekkum, and D. Valerio. "Expression of human adenosine deaminase in mice transplanted with hemopoietic stem cells infected with amphotropic retroviruses." Journal of Experimental Medicine 172, no. 3 (September 1, 1990): 729–36. http://dx.doi.org/10.1084/jem.172.3.729.

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Amphotropic recombinant retroviruses were generated carrying sequences encoding human adenosine deaminase (ADA). Transcription of the human ADA gene was under control of a hybrid long terminal repeat in which the enhancer from the Moloney murine leukemia virus was replaced by an enhancer from the F101 host-range mutant of polyoma virus. Hemopoietic stem cells in murine bone marrow were infected with this virus under defined culture conditions. As a result, 59% of day-12 colony forming unit spleen (CFU-S) stem cells became infected without any in vitro selection. Infected CFU-S were shown to express human ADA before transplantation and this expression sustained upon in vivo maturation. Mice transplanted with infected bone marrow exhibited human ADA expression in lymphoid, myeloid, and erythroid cell types. Moreover, human ADA expression persisted in secondary and tertiary transplanted recipients showing that human ADA-expressing cells were derived from pluripotent stem cells. These characteristics of our amphotropic viruses make them promising tools in gene therapy protocols for the treatment of severe combined immunodeficiency caused by ADA deficiency. In this respect it is also relevant that the viral vector that served as backbone for the ADA vector was previously shown to be nonleukemogenic.

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10

Barrette, Stephane, Janet L. Douglas, Nancy E. Seidel, and David M. Bodine. "Lentivirus-based vectors transduce mouse hematopoietic stem cells with similar efficiency to Moloney murine leukemia virus–based vectors." Blood 96, no. 10 (November 15, 2000): 3385–91. http://dx.doi.org/10.1182/blood.v96.10.3385.

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Abstract The low levels of transduction of human hematopoietic stem cells (HSCs) with Moloney murine leukemia virus (MLV) vectors have been an obstacle to gene therapy for hematopoietic diseases. It has been demonstrated that lentivirus vectors are more efficient than MLV vectors at transducing nondividing cell lines as well as human CD34+ cells and severe combined immunodeficiency disease repopulating cells. We compared transduction of cell lines and Lin− bone marrow cells, using a vesicular stomatitis virus G (VSV-G)-pseudotyped lentivirus or MLV vectors carrying a green fluorescent protein marker gene. As predicted, the lentivirus vector was more efficient at transducing mouse and human growth-inhibited cell lines. The transduction of mouse HSC by lentivirus vectors was compared directly to MLV vectors in a co-transduction assay. In this assay, transduction by ecotropic MLV is a positive internal control for downstream steps in retrovirus transduction, including cell division. Both the VSV-G lentivirus and MLV vectors transduced mouse HSCs maintained in cytokine-free medium at very low frequency, as did the ecotropic control. The lentivirus vector and the MLV vector were equally efficient at transducing bone marrow HSCs cultured in interleukin 3 (IL-3), IL-6, and stem cell factor for 96 hours. In conclusion, although lentivirus vectors are able to transduce growth-inhibited cell lines, the cell cycle status of HSCs render them resistant to lentivirus-mediated transduction, and it is hypothesized that entry into cycle, not necessarily division, may be a requirement for efficient lentivirus-mediated transduction.

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Dissertations / Theses on the topic "Moloney murine leukemia virus; Therapy"

1

Ismail, Said. "Development of novel MoMLV gene transfer systems by exploiting retroviral RNA processing." Thesis, University of Oxford, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365806.

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2

Vasser, Geneva M. "Manipulation of the moloney murine leukemia virus envelope protein in an effort to develop directly and indirectly targeted retroviral vectors for use in human gene therapy." View the abstract Download the full-text PDF version, 2008. http://etd.utmem.edu/ABSTRACTS/2008-031-Vasser-Index.html.

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Thesis (M.S. )--University of Tennessee Health Science Center, 2008
Title from title page screen (viewed on Sept. 17, 2008). Research advisor: Lorraine M. Albritton, Ph.D. Document formatted into pages (x, 138 p. : ill.). Vita. Abstract. Includes bibliographical references (p. 40-48).

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3

Wallin, Michael. "Fusion activation in murine leukemia virus /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-748-0/.

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Koepke, Kristine Ann. "Expression and characterization of integrase from Moloney murine leukemia virus." Thesis, University of Bath, 1994. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359638.

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Klimowicz, Alexander Charles. "Pseudotyping the Moloney murine leukemia virus with engineered envelope glycoproteins." Thesis, University of Ottawa (Canada), 2001. http://hdl.handle.net/10393/9297.

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We were interested in generating an in vivo retroviral gene therapy vector based on the commonly used Moloney murine leukemia virus (MoMLV). This was accomplished by pseudotyping with an engineered influenza A hemagglutinin. Point mutations were introduced to abrogate hemagglutinin's wild type binding and a single chain variable domain antibody fragment (scFv) was added to its amino terminus to provide new binding specificity. The engineered hemagglutinin was able to mediate binding of pseudotyped retrovirus to a scFv specific peptide but was unable mediate infection of target cells. To rescue the infectivity of the pseudotyped retrovirus the role of lipid rafts in the lifecycle of the MoMLV was examined. Lipid raft isolation from transfected cells and virus particles revealed that retroviral proteins were not associated with lipid rafts. Using a panel of hemagglutinin mutants with reduced lipid raft affinity we also determined that this parameter did not affect pseudotyping efficiency.

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Hamirally, Sofia. "Mechanistic studies of the translational readthrough signal of Moloney murine leukemia virus." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.619933.

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7

Villeneuve, Luc. "Insertional mutagenesis by provirus integration in Moloney murine leukemia virus-induced rat thymomas." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=74060.

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Konishi, Atsushi. "Studies on the thermostabilization of reverse transcriptases from Moloney murine leukemia virus and avian myeloblastosis virus." Kyoto University, 2015. http://hdl.handle.net/2433/199340.

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Kyoto University (京都大学)
0048
新制・課程博士
博士(農学)
甲第19016号
農博第2094号
新制||農||1029(附属図書館)
学位論文||H27||N4898(農学部図書室)
31967
京都大学大学院農学研究科食品生物科学専攻
(主査)教授保川清, 教授河田照雄, 教授谷史人
学位規則第4条第1項該当

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Bae, Youngmee. "Study on the surface protein of Moloney murine leukaemia virus (Mo-MuLV), GP70." Thesis, University of Oxford, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320614.

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Zedeler, Anne. "Palmitoylation and raft localization of the retrovirus Moloney MLV R-peptide studied by mutagenesis : PhD thesis /." Cph. : Department of Pharmacology, The Danish University of Pharmaceutical Sciences, 2005. http://www.dfuni.dk/index.php/Anne_Zedeler/1733/0/.

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Book chapters on the topic "Moloney murine leukemia virus; Therapy"

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Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "Provirus Insertion Site of Moloney Murine Leukemia Virus 1 Pim-1." In Encyclopedia of Signaling Molecules, 1488. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101109.

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Wong, P. K. Y. "Moloney Murine Leukemia Virus Temperature-Sensitive Mutants: A Model for Retrovirus-Induced Neurologic Disorders." In Current Topics in Microbiology and Immunology, 29–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75267-4_3.

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Wong, Paul K. Y., and P. H. Yuen. "Molecular Basis of Neurologic Disorders Induced by a Mutant, ts1, of Moloney Murine Leukemia Virus." In Molecular Neurovirology, 161–97. Totowa, NJ: Humana Press, 1992. http://dx.doi.org/10.1007/978-1-4612-0407-7_3.

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Flyer, David C., Douglas V. Faller, and Steven J. Burakoff. "Antigenic Requirements for the Recognition of Moloney Murine Leukemia Virus-Induced Tumors by Cytotoxic T Lymphocytes." In Development and Recognition of the Transformed Cell, 221–30. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1925-2_14.

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Villar, C. J., T. N. Fredrickson, and C. A. Kozak. "Effect of the Gv-1 Locus on Moloney Ecotropic Murine Leukemia Virus Induced Disease in Inbred Wild Mice." In Genetics of Immunological Diseases, 250–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-50059-6_38.

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Shaughnessy, J., K. Huppi, J. F. Mushinski, and M. Potter. "Moloney Murine Leukemia Virus Integration 1060 Base Pairs 5’ of c-myc Exon 1 in a Plasmacytoma Without a Chromosomal Translocation." In Current Topics in Microbiology and Immunology, 303–6. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-75889-8_37.

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"Moloney Murine Leukemia Virus." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1248. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_10676.

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Menéndez-Arias, Luis, József Tözsér, and Stephen Oroszlan. "Moloney murine leukemia virus retropepsin." In Handbook of Proteolytic Enzymes, 176–78. Elsevier, 2004. http://dx.doi.org/10.1016/b978-0-12-079611-3.50058-6.

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"MoMuLV (Moloney murine leukemia virus)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 1249. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_10681.

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Menéndez-Arias, Luis, József Tözsér, and Stephen Oroszlan. "Moloney Murine Leukemia Virus Retropepsin." In Handbook of Proteolytic Enzymes, 226–30. Elsevier, 2013. http://dx.doi.org/10.1016/b978-0-12-382219-2.00053-3.

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