Academic literature on the topic 'Virus mpsv'
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Journal articles on the topic "Virus mpsv"
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Seliger, B., R. Kollek, C. Stocking, T. Franz, and W. Ostertag. "Viral transfer, transcription, and rescue of a selectable myeloproliferative sarcoma virus in embryonal cell lines: expression of the mos oncogene." Molecular and Cellular Biology 6, no. 1 (January 1986): 286–93. http://dx.doi.org/10.1128/mcb.6.1.286.
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A derivative of the myeloproliferative sarcoma virus (Neor-MPSV) carrying the mos oncogene and dominant selection marker for neomycin resistance (Neor) was introduced into embryonal carcinoma and embryo-derived cell lines by transfection and infection using pseudotypes with Friend helper virus (Friend murine leukemia virus [F-MuLV]). Cells resistant to G418 (a neomycin analog) were cloned and expanded. Transductants retained an undifferentiated phenotype as judged by morphology, tumorigenicity, and cell-surface antigen analyses. Nucleic acid analysis of infectants revealed both Neor-MPSV and F-MuLV proviruses, although no virus was released. G418-resistant transductants remained nonpermissive for the expression of other proviruses and for subsequent superinfection. Northern analysis showed expression of full-length Neor-MPSV, as well as mos-specific subgenomic RNA. mos sequences were deleted from Neor-MPSV (Neor mos-1), and pseudotypes were used to infect embryonal carcinoma cells. No morphological differences were observed in either mos+ or mos- transductants as compared with parental cell lines. However, mos+ transductants showed an enhanced anchorage-independent growth compared with that of mos- transductants in agar cloning. PCC4 transductants were induced to differentiate with retinoic acid and superinfected with F-MuLV. Infection with viral supernatant in fibroblasts and in mice confirmed the rescue of biologically active Neor-MPSV.
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Onodera, Masafumi, David M. Nelson, Akihiro Yachie, G. Jayashree Jagadeesh, Bruce A. Bunnell, Richard A. Morgan, and R. Michael Blaese. "Development of Improved Adenosine Deaminase Retroviral Vectors." Journal of Virology 72, no. 3 (March 1, 1998): 1769–74. http://dx.doi.org/10.1128/jvi.72.3.1769-1774.1998.
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ABSTRACT A series of adenosine deaminase (ADA) retroviral vectors were designed and constructed with the goal of improved performance over the PA317/LASN vector currently used in clinical trials. First, the bacterial selectable-marker neomycin phosphotransferase (neo) gene was removed to create a “simplified” vector. Second, the Moloney murine leukemia virus long terminal repeat (LTR) promoter used for ADA expression was replaced with either the myeloproliferative sarcoma virus (MPSV) or SL3-3 LTR. Supernatant from each ADA vector was used to transduce ADA-deficient (ADA−) B- and T-cell lines as well as primary peripheral blood mononuclear cells (PBMC) from an ADA− severe combined immunodeficiency patient. Total ADA enzyme activity and ADA activity per integrant in the transduced cells demonstrated that the MPSV LTR splicing vector design provided the highest level of ADA expression per cell. This ADA(MPSV) vector was then tested in packaging cell lines containing either the gibbon ape leukemia virus envelope (PG13 cells), the murine amphotropic envelope (FLYA13 cells), or the feline endogenous virus RD114 envelope (FLYRD18 cells). The results indicate that FLYRD18/ADA(MPSV), a simplified ADA retroviral vector with the MPSV LTR, provides a 17-fold-higher level of ADA expression in human lymphohematopoietic cells than the PA317/LASN vector currently in use.
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Seliger, B., R. Kollek, C. Stocking, T. Franz, and W. Ostertag. "Viral transfer, transcription, and rescue of a selectable myeloproliferative sarcoma virus in embryonal cell lines: expression of the mos oncogene." Molecular and Cellular Biology 6, no. 1 (January 1986): 286–93. http://dx.doi.org/10.1128/mcb.6.1.286-293.1986.
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A derivative of the myeloproliferative sarcoma virus (Neor-MPSV) carrying the mos oncogene and dominant selection marker for neomycin resistance (Neor) was introduced into embryonal carcinoma and embryo-derived cell lines by transfection and infection using pseudotypes with Friend helper virus (Friend murine leukemia virus [F-MuLV]). Cells resistant to G418 (a neomycin analog) were cloned and expanded. Transductants retained an undifferentiated phenotype as judged by morphology, tumorigenicity, and cell-surface antigen analyses. Nucleic acid analysis of infectants revealed both Neor-MPSV and F-MuLV proviruses, although no virus was released. G418-resistant transductants remained nonpermissive for the expression of other proviruses and for subsequent superinfection. Northern analysis showed expression of full-length Neor-MPSV, as well as mos-specific subgenomic RNA. mos sequences were deleted from Neor-MPSV (Neor mos-1), and pseudotypes were used to infect embryonal carcinoma cells. No morphological differences were observed in either mos+ or mos- transductants as compared with parental cell lines. However, mos+ transductants showed an enhanced anchorage-independent growth compared with that of mos- transductants in agar cloning. PCC4 transductants were induced to differentiate with retinoic acid and superinfected with F-MuLV. Infection with viral supernatant in fibroblasts and in mice confirmed the rescue of biologically active Neor-MPSV.
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Le Bousse-Kerdiles, MC, M. Souyri, F. Smadja-Joffe, V. Praloran, C. Jasmin, and HJ Ziltener. "Enhanced hematopoietic growth factor production in an experimental myeloproliferative syndrome." Blood 79, no. 12 (June 15, 1992): 3179–87. http://dx.doi.org/10.1182/blood.v79.12.3179.3179.
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Abstract The murine myeloproliferative syndrome induced by the myeloproliferative sarcoma virus (MPSV) has numerous similarities to human primary myelofibrosis. We have shown that medium conditioned by spleen cells of MPSV-infected mice has the capacity to support the growth of primitive blast cell colonies. The detection of this activity associated with MPSV infection stimulated us to characterize the hematopoietins responsible for this activity. Northern blot analysis showed a large increase, or induction, of interleukin-6 (IL-6), granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage- CSF (CSF-1), and granulocyte-CSF (G-CSF) transcripts in the hematopoietic organs of MPSV-infected mice; however, no IL-3 transcript could be detected in either MPSV-infected or normal mice. Significant levels of IL-1 alpha, IL-6, G-CSF, and CSF-1 bioactivities were found in the serum of MPSV-infected mice, but not in controls. Additionally, analysis of medium conditioned by spleen cells of MPSV-infected mice showed the presence of tumor necrosis factor alpha bioactivity. The increased production of cytokines that are able to stimulate pluripotent hematopoietic stem cells corroborates the hypothesis of a possible involvement of hematopoietic growth factors in the development of some myeloproliferative disorders.
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Le Bousse-Kerdiles, MC, M. Souyri, F. Smadja-Joffe, V. Praloran, C. Jasmin, and HJ Ziltener. "Enhanced hematopoietic growth factor production in an experimental myeloproliferative syndrome." Blood 79, no. 12 (June 15, 1992): 3179–87. http://dx.doi.org/10.1182/blood.v79.12.3179.bloodjournal79123179.
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The murine myeloproliferative syndrome induced by the myeloproliferative sarcoma virus (MPSV) has numerous similarities to human primary myelofibrosis. We have shown that medium conditioned by spleen cells of MPSV-infected mice has the capacity to support the growth of primitive blast cell colonies. The detection of this activity associated with MPSV infection stimulated us to characterize the hematopoietins responsible for this activity. Northern blot analysis showed a large increase, or induction, of interleukin-6 (IL-6), granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage- CSF (CSF-1), and granulocyte-CSF (G-CSF) transcripts in the hematopoietic organs of MPSV-infected mice; however, no IL-3 transcript could be detected in either MPSV-infected or normal mice. Significant levels of IL-1 alpha, IL-6, G-CSF, and CSF-1 bioactivities were found in the serum of MPSV-infected mice, but not in controls. Additionally, analysis of medium conditioned by spleen cells of MPSV-infected mice showed the presence of tumor necrosis factor alpha bioactivity. The increased production of cytokines that are able to stimulate pluripotent hematopoietic stem cells corroborates the hypothesis of a possible involvement of hematopoietic growth factors in the development of some myeloproliferative disorders.
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Laker, C., G. Gräning, A. Kelso, C. Stocking, and W. Ostertag. "Abrogation of the requirement for feeder cell interaction and T cell receptor stimulation of lymphocytes infected with retroviral vectors." Journal of Experimental Medicine 172, no. 2 (August 1, 1990): 447–56. http://dx.doi.org/10.1084/jem.172.2.447.
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Infection of sensitive adult mice with myeloproliferative sarcoma virus (MPSV) results in a myeloproliferative syndrome. Two components of the viral genome are required to induce this unique pathology: the mos oncogene and sequences within the U3 region of the long terminal repeat (LTR). In studies designed to identify the target cell of MPSV and thus better understand the mechanism by which a myeloproliferative syndrome is induced, we have infected a series of T cell lines with MPSV-based vectors. The results presented here show that infection with neoR MPSV abrogates the requirement for an antigen-specific or feeder cell-dependent stimulation, without altering the requirement for interleukin 2. Significantly, this response is not dependent on the mos oncogene, but requires sequences within the U3 region of the MPSV LTR. No alteration in the constitutive or induced levels of lymphokines released by these cells was observed. These results suggest a model in which T cells acquire a proliferative advantage by uncoupling the proliferative response from the lymphokine synthesis that is induced by activation of the T cell receptor. These cells are thus poised for antigen stimulation and secretion of cytokines that stimulate myelopoiesis.
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Allay, JA, LL Dumenco, ON Koc, L. Liu, and SL Gerson. "Retroviral transduction and expression of the human alkyltransferase cDNA provides nitrosourea resistance to hematopoietic cells." Blood 85, no. 11 (June 1, 1995): 3342–51. http://dx.doi.org/10.1182/blood.v85.11.3342.bloodjournal85113342.
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Myelosuppression is the dose-limiting toxicity for nitrosourea chemotherapy. This toxicity predominantly involves modification of the O6 position of guanine with an alkyl moiety. The enzyme responsible for repair of O6-alkylguanine adducts, O6-alkylguanine-DNA alkyltransferase (alkyltransferase), is expressed at low levels in bone marrow (BM) cells. High alkyltransferase expression prevents the cytotoxicity and carcinogenicity of nitrosoureas in several transgenic and in vitro gene transfer models. We used gene transfer using a novel myeloproliferative sarcoma virus (MPSV) based retrovirus (vM5MGMT) to express the human alkyltransferase cDNA (MGMT) in human and murine hematopoietic cells. Transduced K562 cells had very high levels of alkyltransferase expression and significantly increased resistance to 1,3-bis (2-chloroethyl) nitrosourea (BCNU) as compared with untransduced K562 cells. Primary murine BM progenitors showed a high transduction efficiency with vM5MGMT and have increased BCNU resistance in vitro. After BM transplantation with vM5MGMT-transduced BM cells and BCNU treatment of these mice, BM, spleen and thymus had a 10- to 40-fold increase in alkyltransferase expression that persisted for at least 23 weeks posttransplantation. Progenitor cells procured from mice expressing high levels of alkyltransferase also had increased resistance to BCNU. Thus, an MPSV-based retroviral vector transduces mouse and human hematopoietic cells at high efficiency and results in high levels of gene expression both in vitro and in vivo. Overexpression of the alkyltransferase protein may protect hematopoietic progenitors from nitrosourea-induced myelosuppression.
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Hayashi, Y., T. Tange, Y. Urano, F. Smadja-Joffe, M. C. Le Bousse-Kerdiles, and C. Jasmin. "Histopathologic Studies on Myeloproliferative Sarcoma Virus (MPSV) Induced Leukemias and Hemangiosarcoma in Jar-2 Rats." Pathology - Research and Practice 183, no. 3 (June 1988): 314–20. http://dx.doi.org/10.1016/s0344-0338(88)80128-6.
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Chinnasamy, Dhanalakshmi, Nachimuthu Chinnasamy, Melissa J. Enriquez, Makoto Otsu, Richard A. Morgan, and Fabio Candotti. "Lentiviral-mediated gene transfer into human lymphocytes: role of HIV-1 accessory proteins." Blood 96, no. 4 (August 15, 2000): 1309–16. http://dx.doi.org/10.1182/blood.v96.4.1309.
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Abstract Resting lymphocytes are refractory to gene transfer using Moloney murine leukemia virus (MMLV)-based retroviral vectors because of their quiescent status. Recently, it has been shown that lentiviral vectors are capable of transferring genes into nondividing and terminally differentiated cells. We used human immunodeficiency virus type-1 (HIV-1)–based vectors expressing enhanced green fluorescent protein (EGFP) driven by different promoters (CMV, MPSV, or PGK) and investigated their ability to transduce human T- and B-cell lines, as well as resting or activated primary peripheral and umbilical cord blood lymphocytes. The effects of the presence or the absence of HIV-1 accessory proteins (Vif, Vpr, Vpu, and Nef) in the vector system were also assessed. Flow cytometry analysis showed no differences in the ability of these vectors of transferring the reporter gene into lymphocytic lines and mitogen-stimulated primary lymphocytes in the presence or the absence of HIV-1 accessory proteins (APs). Similarly, viral supernatants generated in the presence of accessory genes could efficiently transduce various subsets of resting lymphocytes and provide long-term expression of the transgene. No significant transduction-induced changes in cell activation or cycling status were observed and Alu-HIV-1 long terminal repeat polymerase chain reaction (LTR PCR) analysis demonstrated integration of the vector sequences at the molecular level. In contrast, in the absence of HIV-1 APs, lentiviral vectors failed to integrate and express the transgene in resting lymphocytes. These results show that transduction of primary resting lymphocytes with HIV-1–based vectors requires the presence of viral accessory proteins.
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Chinnasamy, Dhanalakshmi, Nachimuthu Chinnasamy, Melissa J. Enriquez, Makoto Otsu, Richard A. Morgan, and Fabio Candotti. "Lentiviral-mediated gene transfer into human lymphocytes: role of HIV-1 accessory proteins." Blood 96, no. 4 (August 15, 2000): 1309–16. http://dx.doi.org/10.1182/blood.v96.4.1309.h8001309_1309_1316.
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Resting lymphocytes are refractory to gene transfer using Moloney murine leukemia virus (MMLV)-based retroviral vectors because of their quiescent status. Recently, it has been shown that lentiviral vectors are capable of transferring genes into nondividing and terminally differentiated cells. We used human immunodeficiency virus type-1 (HIV-1)–based vectors expressing enhanced green fluorescent protein (EGFP) driven by different promoters (CMV, MPSV, or PGK) and investigated their ability to transduce human T- and B-cell lines, as well as resting or activated primary peripheral and umbilical cord blood lymphocytes. The effects of the presence or the absence of HIV-1 accessory proteins (Vif, Vpr, Vpu, and Nef) in the vector system were also assessed. Flow cytometry analysis showed no differences in the ability of these vectors of transferring the reporter gene into lymphocytic lines and mitogen-stimulated primary lymphocytes in the presence or the absence of HIV-1 accessory proteins (APs). Similarly, viral supernatants generated in the presence of accessory genes could efficiently transduce various subsets of resting lymphocytes and provide long-term expression of the transgene. No significant transduction-induced changes in cell activation or cycling status were observed and Alu-HIV-1 long terminal repeat polymerase chain reaction (LTR PCR) analysis demonstrated integration of the vector sequences at the molecular level. In contrast, in the absence of HIV-1 APs, lentiviral vectors failed to integrate and express the transgene in resting lymphocytes. These results show that transduction of primary resting lymphocytes with HIV-1–based vectors requires the presence of viral accessory proteins.
Dissertations / Theses on the topic "Virus mpsv"
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Le, Bousse-Kerdiles Caroline. "Etude physiopathologique du syndrome myeloproliferatif provoque par le virus sarcomatogene myeloproliferatif murin : mise en evidence d'une activite stimulant la proliferation et la differenciation des cellules souches hematopoietiques pluripotentes." Paris 7, 1987. http://www.theses.fr/1987PA077220.
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SONGO, PIERRE. "Sida : analyse genomique des retrovirus hiv 1 et 2, siv, visna et mpmv." Paris 7, 1988. http://www.theses.fr/1988PA077157.
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BENIT, LAURENCE. "Determinants genetiques de la pathogenese du mplv (myelo proliferative leukemia virus)." Paris 7, 1994. http://www.theses.fr/1994PA077203.
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Le myeloproliferative leukemia virus (mplv), est un retrovirus defectif a oncogene, responsable d'un syndrome myeloproliferatif aigu chez la souris. Le gene de fusion env-mpl qu'il porte code pour une version du recepteur a la thrombopoietine profondement remaniee. Le domaine extracellulaire du recepteur viral comporte une premiere portion codee par la sequence remaniee d'enveloppe, suivie d'une courte sequence v-mpl (43 acides amines au lieu de 485 dans la proteine c-mpl). Les regions membranaire et cytoplasmique sont entierement codees par la portion v-mpl, equivalentes a celles de la proteine c-mpl. Cette these a porte essentiellement sur la recherche des determinants genetiques de la pathogenese du mplv. Nous avons montre dans un premier temps que ces determinants sont contenus dans le gene de fusion env-mpl. Dans un second temps, nous avons delimite les regions minimales de la proteine env-mpl requises pour la pathologie. Nous avons montre que dans la region extracellulaire, le motif ws tres conserve dans la famille des recepteurs de cytokines a laquelle appartient c-mpl, n'est pas necessaire a la pathologie du mplv. Le remaniement et la deletion interne du gene d'enveloppe n'interviennent pas non plus dans cette pathologie. Dans le domaine cytoplasmique, la sequence minimale indispensable comporte les 69 premiers acides amines (sur 119 au total). On trouve dans cette region des motifs connus pour leur role dans la transmission des signaux proliferatifs delivres par les recepteurs de cytokines. Ces motifs sont les boites 1 et 2, ainsi que des residus acides. La region carboxy-terminale (22 derniers acides amines) pourrait jouer un role dans une activite du recepteur, autre que proliferative. Ceci a ete observe dans l'induction de proteines de la phase aigue de l'inflammation. L'etude d'un variant pathogenique du mplv a montre que l'activation du recepteur oncogenique env-mpl et/ou de la proteine c-mpl pourrait mettre en jeu la formation de dimeres, comme c'est le cas pour un certain nombre de recepteurs de cytokines. Dans des experiences menees ex-vivo, nous avons montre que l'activation de v-mpl et de c-mpl, est associee a celle de proteines jak et stat, qui interviennent dans la signalisation cellulaire
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Vigon, Isabelle. "Clonage moleculaire du virus leucemogene myeloproliferatif murin (mplv). Isolement et caracterisation des homologues cellulaires humains et murins de l'oncogene v-mpl transduit par le mplv." Paris 7, 1992. http://www.theses.fr/1992PA077297.
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Le virus leucemogene myeloproliferatif murin ou mplv est un retrovirus leucemogene murin qui provoque in vivo un syndrome myeloproliferatif aigu. In vitro, il entraine l'immortalisation de precurseurs des differentes lignees hematopoietiques qui proliferent et se differencient en l'absence de facteurs de croissance. Le mplv derive du virus f-mulv dont il differe par sa region enveloppe fortement remaniee. Un provirus mplv biologiquement actif a ete clone moleculairement. L'analyse de la sequence de son gene enveloppe a montre qu'il a subi deux deletions et qu'il contient une sequence non virale nommee v-mpl. Cette sequence, conservee chez les mammiferes, a ete localisee sur le chromosome 4 de la souris et en 1p34 chez l'homme. Mpl ne correspond a aucun gene connu mais appartient a la superfamille des recepteurs de facteurs de croissance hematopoietiques depourvus d'activite kinase. Le gene c-mpl est exprime dans les organes hematopoietiques. Des adnc de ce gene ont ete clones chez l'homme et chez la souris. Chez l'homme, deux familles d'adnc ont ete isoles. Ils coderaient pour des proteines differant par leur region cytoplasmique. Chez la souris, des clones codant pour une proteine transmembranaire ou pour une proteine soluble ont ete isoles. Ces differents adnc sont probablement generes par epissages alternatifs et certaines de ces formes pourraient moduler la fonction normale du recepteur ou intervenir de facon differente dans la transmission du signal par ce recepteur. Le v-mpl est une version fortement tronquee mais non mutee du c-mpl murin. Il s'agit du premier exemple de transduction retrovirale d'un gene de la superfamille des recepteurs de facteurs de croissance hematopoietiques
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Sabaliauskaitė, Rasa. "Chimerinių pelių poliomos viruso paviršiaus VP1 baltymų, eksponuojančių HCV epitopus, konstravimas." Master's thesis, Lithuanian Academic Libraries Network (LABT), 2010. http://vddb.laba.lt/obj/LT-eLABa-0001:E.02~2007~D_20101125_183215-91788.
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Magistrinio darbo metu sukonstruotos mielių plazmidės, turinčios pelių poliomos viruso pagrindinį kapsidės baltymą VP1 su jame įterptais hepatito C viruso apvalkalo baltymų peptidais. Šiomis plazmidėmis buvo transformuotos S. cerevisiae mielės. Transformuotos mielės sintetina chimerinius baltymus: MPyV-VP1-BC-E2 [384-414], MPyV-VP1-HI-E2 [384-414], MPyV-VP1-BC-E1 [310-329], MPyV-VP1-HI-E1 [310-329], MPyV-VP1-BC-E2 [412-i447], MPyV-VP1-HI-E2 [412-i447], MPyV-VP1-BC-E1 [310-329]-HI-E2 [412-447], MPyV-VP1-BC-E1 [310-329]-HI-E2 [412-i447], MPyV-VP1-BC-E2 [412-447]-HI-E1 [310-329], MPyV-VP1-BC-E2 [412-i447]-HI-E1 [310-329]. Į virusus panašias daleles (VPD) renkasi tik MPyV-VP1-BC-E2 [384-414], MPyV-VP1-HI-E2 [384-414], MPyV-VP1-BC-E1 [310-329] baltymai. Kiti baltymai: MPyV-VP1-BC-E1 [310-329], MPyV-VP1-HI-E1 [310-329], MPyV-VP1-BC-E2 [412-i447], MPyV-VP1-HI-E2 [412-i447], MPyV-VP1-BC-E1 [310-329]-HI-E2 [412-447], MPyV-VP1-BC-E1 [310-329]-HI-E2 [412-i447], MPyV-VP1-BC-E2 [412-447]-HI-E1 [310-329], MPyV-VP1-BC-E2 [412-i447]-HI-E1 [310-329] nesirinko į VPD.In the present study, plasmids for expression of major capsid proteins VP1 of murine polyomavirus with inserted sequences from Hepatitis C virus envelope proteins in yeast S. cerevisiae were constructed. The plasmids were used to transform yeast cells. The transformed yeast produced proteins: MPyV-VP1-BC-E2 [384-414], MPyV-VP1-HI-E2 [384-414], MPyV-VP1-BC-E1 [310-329], MPyV-VP1-HI-E1 [310-329], MPyV-VP1-BC-E2 [412-i447], MPyV-VP1-HI-E2 [412-i447], MPyV-VP1-BC-E1 [310-329]-HI-E2 [412-447], MPyV-VP1-BC-E1 [310-329]-HI-E2 [412-i447], MPyV-VP1-BC-E2 [412-447]-HI-E1 [310-329], MPyV-VP1-BC-E2 [412-i447]-HI-E1 [310-329]. Virus-like particles (VLPs) composed MPyV-VP1-BC-E2 [384-414], MPyV-VP1-HI-E2 [384-414], MPyV-VP1-BC-E1 [310-329]. Other proteins: MPyV-VP1-BC-E1 [310-329], MPyV-VP1-HI-E1 [310-329], MPyV-VP1-BC-E2 [412-i447], MPyV-VP1-HI-E2 [412-i447], MPyV-VP1-BC-E1 [310-329]-HI-E2 [412-447], MPyV-VP1-BC-E1 [310-329]-HI-E2 [412-i447], MPyV-VP1-BC-E2 [412-447]-HI-E1 [310-329], MPyV-VP1-BC-E2 [412-i447]-HI-E1 [310-329] did not form VLPs.
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Cubizolle, Aurélie. "Etude de l'efficacité du transfert du gène de la beta-D-glucuronidase dans le SNC de chiens atteints de mucopolysaccharidose de type VII." Thesis, Montpellier 2, 2012. http://www.theses.fr/2012MON20220/document.
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La mucopolysaccharidose de type VII (MPS VII) est une maladie génétique de surcharge lysosomale provoquée par une déficience en β-D-glucuronidase (β-glu). β-glu est impliquée dans la cascade de dégradation et de recyclage des glycosaminoglycannes (GAGs). Sa déficience provoque une accumulation vésiculaire de GAGs non dégradés engendrant in fine la mort cellulaire. Notre but est de développer et de tester la pertinence des vecteurs adénoviraux canins helper-dépendant (HD-CAV-2) pour traiter la neurodégénération provoquée par la MPS VII dans le cadre d'une thérapie génique dans le SNC de chien. Parce que les vecteurs CAV-2 transduisent préférentiellement les neurones et qu'ils sont transportés de manière rétrograde le long des axones, leurs distributions dans tout le SNC permettraient de délivrer largement la β-glu dans tout le parenchyme cérébral. Nous avons alors étudié la sureté, la durée d'expression, l'efficacité et la possible réversion du phénotype après injections dans le SNC de chiens MPS VII d'un HD-CAV-2 exprimant le gène humain de la GUSB : HD-RIGIE. Des études préliminaires ont montré la faisabilité du transfert des vecteurs HD-CAV-2 dans le SNC, qu'ils induisaient une réponse immunitaire minimale et qu'ils transduisaient préférentiellement, efficacement et largement les neurones.Nous avons produit un HD-RIGIE de qualité pour les injections intracérébrales et nous avons analysé son efficacité sur l'accumulation de GAGs non dégradés. Les injections de HD-RIGIE montrent une augmentation générale de l'activité β-glu dans tout le SNC des chiens MPS VII (sites d'injections et structures éloignées comme le cortex) et ce 1 mois ou 4 mois après les injections. L'analyse de la GFP confirme une distribution globale de HD-RIGIE dans le SNC d'animaux de grande taille. De plus, grâce aux propriétés intrinsèques de la β-glu (transport rétrograde et phénomène de libération/recapture), nous avons observé une diminution générale de l'accumulation vésiculaire neuronale des GAGs non dégradés dans tout le parenchyme cérébral. D'autre part grâce à la stratégie d'isolement et de non vaccination des chiens MPS VII, nous n'observons ni de réponse immunitaire humorale, ni d'aggravation de l'inflammation du parenchymeMucopolysaccharidosis type VII (MPS VII) is a rare inherited lysosomal storage disease caused by β-D-glucuronidase (β-glu) deficiency. β-glu is involved in the physiological turnover of glycosaminoglycans (GAGs). Its deficiency causes accumulation of undegraded GAGs inside vesicles leading to cell death. Our goals are to develop and test the clinical relevance of helper-dependant (HD) canine adenovirus type 2 (CAV-2) vectors to treat neural degeneration caused by MPS VII in a dog model. Because CAV-2 targets preferentially neurons and traffics via axons, the distribution of the transgene throughout the CNS will allow widespread delivery of the missing lysosomal enzyme in these disorders with a minimum number of injections. We tested a HD-CAV-2 vector expressing the human GUS gene in the canine model of MPS VII for their safety, efficacy, duration of expression and possible reversion of the MPS VII induced symptoms.A previous study based on HD-CAV-EGFP vector injections in MPS VII-/- and healthy dogs showed that we are now able to inject HD-CAV-2 in the dog brain, have a minimal induction of the immune response, an efficient transduction of the neurons and an efficient biodistribution of transduced cells. After the production of a suitable vector (HD-RIGIE) for injections in the CNS of MPS VII dogs we analysed its efficiency on GAGS storage in neurons.Injections of HD-RIGIE showed after 1 month or 4 months post injections a widespread increase in general level of β-glu activity, in the sites of injections and in distant areas such as cortex. Analysis of GFP, also permit to observe a widespread biodistribution of the vector. Because of β-glu property of cross-correction we observed a global decreased in GAGs storage in the entire MPS VII brains. Finally, the dogs did not present humoral immune response and no aggravation of inflammation
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Verdánová, Martina. "Interakce polyomavirů s proteazomálním systémem hostitelských buněk." Master's thesis, 2011. http://www.nusl.cz/ntk/nusl-312471.
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Interaction of polyomaviruses with proteasomal system of host cells Abstract: Viral family Polyomaviridae includes besides model organisms - mouse polyomavirus and SV40 virus, also human pathogens, for example, BK virus. Polyomaviruses are small non- enveloped viruses with double-stranded DNA. Understanding of their life cycle is important for their use in gene therapy and immunotherapy as well as for prevention and treatment of complications caused by these viruses. This thesis is focused on early phases of MPyV and SV40 infection studying, mainly on delivery of viral genome to nucleus and role of proteasomal system in this stage of infection. It was found out that inhibition of proteasomes by specific inhibitor leads to increase of early non-structural protein LT expression, which was chosen as marker for viral entry to the nucleus and successful viral expression. Relative localization of proteasomes and VP1 protein of MPyV and SV40 was monitored and it showed 10% colocalization of mentioned structures. Further, it was found out that proteasomal inhibitor MG-132 negatively influences the replication of both viral and cellular DNA. Next aim of this diploma thesis was to prepare antigen - unique part of VP2 protein of BKV - for producing antibody. Expression vector with inserted fragment of unique part of...
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Wang, Ko-Wei, and 王克偉. "Development of the Multiplex PCR Assays for Mouse Parvovirus (MPV) and Minute Virus of Mice (MVM), and the Surveillance of MPV and MVM Infection in Laboratory Mice in Taiwan." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/08884927380518379075.
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碩士國立臺灣大學
獸醫學研究所
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Mouse parvoviruses are among the highly prevalent infectious pathogens in contemporary mouse colonies. There are two serotypes, minute virus of mice (MVM) and mouse parvovirus (MPV). Mouse parvoviruses have a predilection for mitotically active cells and can interfere with immunology, transplantation, and oncology research through virus-infected rodents, contaminated cells and biological materials. In order to detect these two viruses simultaneously, a multiplex PCR assay that amplifies the VP gene of MPV and MVM, and a mouse housekeeping gene has been developed in this study. The MPV/MVM/Actin Multiplex PCR assay specifically detects MPV and MVM, but doesn’t amplify KRV, RMV-1, RPV-1c, and H-1. The multiplex PCR assay could simultaneously detect both MVM and MPV in as low as 50 copies in the condition of equal-amount dual infection. The sensitivity of this multiplex PCR assay remained to detect at least 50 copies of MPV when the copies of MVM were 200 times higher than the MPV copy number, and vice versa. The prevalence surveillance result revealed that 3 out of 7 laboraotry mouse colonies were contaminated with MPV with the prevalence of 11.5%; however, none of the tested mouse colony was contaminated with MVM. The MPV/MVM/Actin Multiplex PCR assay developed in this study can provide a useful tool in the mouse health monitoring in the future.
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Hron, Tomáš. "Vývoj experimentálního systému založeného na Cre/LoxP rekombinaci pro produkci polyomavirových mutant." Master's thesis, 2013. http://www.nusl.cz/ntk/nusl-321107.
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Murine polyomavirus is an important member of Polyomaviridae family offering potential applications in gene therapy and immunotherapy. Viral mutant analysis is crucial for study of the virus, however, commonly used methods of its production are laborious and give low yields. This thesis involves development of the new experimental system that can produce intact viral genome from recombinant plasmid in vivo using Cre/loxP-mediated recombination. One loxP site is unavoidably introduced into newly generated viral genome during recombination. Two variants of production plasmids generating wild type viral genome with incorporation of loxP between the poly(A) signal sites of early and late genes or into the intronic region of early genes were prepared. LoxP insertion between the poly(A) signal sites has a dramatic effect on viral gene expression and leads to complete loss of virus infectivity. Conversely, the infectious virus was obtained from the viral genome containing loxP site in the early intronic region. To ensure expression of Cre recombinase I also prepared stably transfected cell lines which can simplify the virus production. This thesis shows that newly designed system gives satisfactory yield of the virus, solves restrictions connected with commonly used methods and can be used for low infectious viral...
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Douville, Renée Nicole. "Asthma, childhood exposures and genetics shape anti-viral cytokine responses in humans." 2007. http://hdl.handle.net/1993/2807.
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Respiratory virus infections are associated with asthma pathogenesis and exacerbations in children and adults. Unfortunately, it remains largely unknown whether innate and adaptive T cell anti-viral immunity differs in allergic disease versus health.
Here, we established a short-term primary cell culture system using human peripheral blood mononuclear cells (PBMC) optimized for measuring immune responses to reovirus, respiratory syncytial virus (RSV) and metapneumovirus (MPV) based on virus-specific cytokine and chemokine production. The prevalence and intensity of innate and adaptive responses in children and adult populations was addressed. Using this in vitro model of human anti-viral immunity, we tested our global hypothesis that asthmatics mount anti-viral cytokine responses to respiratory viruses that differ from those of healthy individuals.
MPV and RSV, although both ubiquitous and leading to very high levels of infection, seroconversion and clinically similar presentation in the population, evoke distinct innate and adaptive T cell-dependent cytokine responses. Reovirus induced exceptionally strong IFN recall responses concomitant with intense IL-10 production, which were independent of viral replication in PBMC.
Surprisingly, despite Type 1 cytokine production dominated adaptive immune responses in both asthmatic and non-asthmatic individuals, asthmatics exhibited significantly stronger pro-inflammatory IFNγ and IL-10 production towards virus stimulation than non-asthmatic children and adults. Moreover, children with current AHR, regardless of asthmatic status, exhibit a greater frequency and intensity of IFNγ responses towards pneumoviruses than do non-AHR counterparts. Conversely, expression of chemokine CCL5 was substantially weaker in asthmatics, and was further decreased in children with AHR and familial history of asthma. This pattern of enhanced pro-inflammatory and deficient anti-viral CCL5 responses towards pneumoviruses in children with markers of symptomatic asthma or AHR may underlie the enhanced sensitivity of these children to experience breathing difficulties following infection with respiratory viruses.
Furthermore, we have clearly demonstrated a gene by environment interaction, whereby ETS exposure in children with familial asthma results in suppressed anti-viral IFNγ and IL-10 production. Therefore, we have attempted to determine whether genetic variation affects the intermediate phenotype of anti-viral immunity, in the population and dependent on clinical status.
In summary, we have demonstrated that asthma, childhood exposures and genetics shape anti-viral cytokine responses in human. These findings have a substantial impact for physicians deciding the contextually appropriate treatment for asthma symptoms in their patients and could have implications for experimentation relating to mechanisms of disease, clinical practice and development of appropriate therapeutics.October 2007
Book chapters on the topic "Virus mpsv"
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Link, Katrin, and Uwe Sonnewald. "Interaction of Movement Proteins with Host Factors, Mechanism of Viral Host Cell Manipulation and Influence of MPs on Plant Growth and Development." In Plant-Virus Interactions, 1–37. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25489-0_1.
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Wendling, Françoise, and Sylvie Gisselbrecht. "The Murine Myeloproliferative Leukemia Virus MPLV, v-mpl Oncogene, and c-mpl." In Thrombopoiesis and Thrombopoietins, 109–22. Totowa, NJ: Humana Press, 1997. http://dx.doi.org/10.1007/978-1-4612-3958-1_6.
Full textConference papers on the topic "Virus mpsv"
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Rouka, Erasmia, Chrissi Hatzoglou, Konstantinos Gourgoulianis, and Sotirios Zarogiannis. "In silico investigation and comparative functional enrichment analysis of the human-respiratory syncytial virus (RSV) and the human-metapneumovirus (MPV) gene interaction networks." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2386.
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