Relevant bibliographies by topics / Virus Cell Fusion

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

Academic literature on the topic 'Virus Cell Fusion'

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Published: 7 September 2023

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Journal articles on the topic "Virus Cell Fusion"

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Leroy, Héloïse, Mingyu Han, Marie Woottum, Lucie Bracq, Jérôme Bouchet, Maorong Xie, and Serge Benichou. "Virus-Mediated Cell-Cell Fusion." International Journal of Molecular Sciences 21, no. 24 (December 17, 2020): 9644. http://dx.doi.org/10.3390/ijms21249644.

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Cell-cell fusion between eukaryotic cells is a general process involved in many physiological and pathological conditions, including infections by bacteria, parasites, and viruses. As obligate intracellular pathogens, viruses use intracellular machineries and pathways for efficient replication in their host target cells. Interestingly, certain viruses, and, more especially, enveloped viruses belonging to different viral families and including human pathogens, can mediate cell-cell fusion between infected cells and neighboring non-infected cells. Depending of the cellular environment and tissue organization, this virus-mediated cell-cell fusion leads to the merge of membrane and cytoplasm contents and formation of multinucleated cells, also called syncytia, that can express high amount of viral antigens in tissues and organs of infected hosts. This ability of some viruses to trigger cell-cell fusion between infected cells as virus-donor cells and surrounding non-infected target cells is mainly related to virus-encoded fusion proteins, known as viral fusogens displaying high fusogenic properties, and expressed at the cell surface of the virus-donor cells. Virus-induced cell-cell fusion is then mediated by interactions of these viral fusion proteins with surface molecules or receptors involved in virus entry and expressed on neighboring non-infected cells. Thus, the goal of this review is to give an overview of the different animal virus families, with a more special focus on human pathogens, that can trigger cell-cell fusion.
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Hernandez, L. D., L. R. Hoffman, T. G. Wolfsberg, and J. M. White. "VIRUS-CELL AND CELL-CELL FUSION." Annual Review of Cell and Developmental Biology 12, no. 1 (November 1996): 627–61. http://dx.doi.org/10.1146/annurev.cellbio.12.1.627.

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Zhang, Chuyuan, Xinjie Meng, and Hanjun Zhao. "Comparison of Cell Fusions Induced by Influenza Virus and SARS-CoV-2." International Journal of Molecular Sciences 23, no. 13 (July 1, 2022): 7365. http://dx.doi.org/10.3390/ijms23137365.

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Virus–cell fusion is the key step for viral infection in host cells. Studies on virus binding and fusion with host cells are important for understanding the virus–host interaction and viral pathogenesis for the discovery of antiviral drugs. In this review, we focus on the virus–cell fusions induced by the two major pandemic viruses, including the influenza virus and SARS-CoV-2. We further compare the cell fusions induced by the influenza virus and SARS-CoV-2, especially the pH-dependent fusion of the influenza virus and the fusion of SARS-CoV-2 in the type-II transmembrane serine protease 2 negative (TMPRSS2-) cells with syncytia formation. Finally, we present the development of drugs used against SARA-CoV-2 and the influenza virus through the discovery of anti-fusion drugs and the prevention of pandemic respiratory viruses.
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Podbilewicz, Benjamin. "Virus and Cell Fusion Mechanisms." Annual Review of Cell and Developmental Biology 30, no. 1 (October 11, 2014): 111–39. http://dx.doi.org/10.1146/annurev-cellbio-101512-122422.

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Muggeridge, Martin I. "Characterization of cell–cell fusion mediated by herpes simplex virus 2 glycoproteins gB, gD, gH and gL in transfected cells." Journal of General Virology 81, no. 8 (August 1, 2000): 2017–27. http://dx.doi.org/10.1099/0022-1317-81-8-2017.

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The mechanisms by which herpes simplex viruses (HSV) mediate fusion between their envelope and the plasma membrane during entry into cells, and between the plasma membranes of adjacent infected and uninfected cells to form multinucleated giant cells, are poorly understood. Four viral glycoproteins (gB, gD, gH and gL) are required for virus–cell fusion, whereas these plus several others are required for cell–cell fusion (syncytium formation). A better understanding would be aided by the availability of a model system, whereby fusion could be induced with a minimal set of proteins, in the absence of infection. A suitable system has now been developed for HSV-2, using transfected COS7, 293 or HEp-2 cells. Insofar as the minimal set of HSV-2 proteins required to cause cell–cell fusion in this system is gB, gD, gH and gL, it would appear to resemble virus–cell fusion rather than syncytium formation. However, the ability of a mutation in gB to enhance the fusion of both transfected cells and infected cells, while having no effect on virus–cell fusion, points to the opposite conclusion. The differential effects of a panel of anti-HSV antibodies, and of the fusion-inhibitor cyclosporin A, confirm that the fusion of transfected cells shares some properties with virus–cell fusion and others with syncytium formation. It may therefore prove useful for determining how these processes differ, and for testing the hypothesis that some viral proteins prevent membrane fusion until the appropriate point in the virus life-cycle, with other proteins then overcoming this block.
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Markosyan, Ruben M., Shan Lu Liu, and Fredric S. Cohen. "Cell-Cell Fusion Mediated by the Fusion Protein of Ebola Virus." Biophysical Journal 106, no. 2 (January 2014): 707a. http://dx.doi.org/10.1016/j.bpj.2013.11.3921.

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Connolly, Sarah A., and Robert A. Lamb. "Paramyxovirus fusion: Real-time measurement of parainfluenza virus 5 virus–cell fusion." Virology 355, no. 2 (November 2006): 203–12. http://dx.doi.org/10.1016/j.virol.2006.07.021.

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Schmid, Erik, Andreas Zurbriggen, Uta Gassen, Bert Rima, Volker ter Meulen, and Jürgen Schneider-Schaulies. "Antibodies to CD9, a Tetraspan Transmembrane Protein, Inhibit Canine Distemper Virus-Induced Cell-Cell Fusion but Not Virus-Cell Fusion." Journal of Virology 74, no. 16 (August 15, 2000): 7554–61. http://dx.doi.org/10.1128/jvi.74.16.7554-7561.2000.

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ABSTRACT Canine distemper virus (CDV) causes a life-threatening disease in several carnivores including domestic dogs. Recently, we identified a molecule, CD9, a member of the tetraspan transmembrane protein family, which facilitates, and antibodies to which inhibit, the infection of tissue culture cells with CDV (strain Onderstepoort). Here we describe that an anti-CD9 monoclonal antibody (MAb K41) did not interfere with binding of CDV to cells and uptake of virus. In addition, in single-step growth experiments, MAb K41 did not induce differences in the levels of viral mRNA and proteins. However, the virus release of syncytium-forming strains of CDV, the virus-induced cell-cell fusion in lytically infected cultures, and the cell-cell fusion of uninfected with persistently CDV-infected HeLa cells were strongly inhibited by MAb K41. These data indicate that anti-CD9 antibodies selectively block virus-induced cell-cell fusion, whereas virus-cell fusion is not affected.
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Zhou, Momei, Vivek Kamarshi, Ann M. Arvin, and Stefan L. Oliver. "Calcineurin phosphatase activity regulates Varicella-Zoster Virus induced cell-cell fusion." PLOS Pathogens 16, no. 11 (November 20, 2020): e1009022. http://dx.doi.org/10.1371/journal.ppat.1009022.

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Cell-cell fusion (abbreviated as cell fusion) is a characteristic pathology of medically important viruses, including varicella-zoster virus (VZV), the causative agent of chickenpox and shingles. Cell fusion is mediated by a complex of VZV glycoproteins, gB and gH-gL, and must be tightly regulated to enable skin pathogenesis based on studies with gB and gH hyperfusogenic VZV mutants. Although the function of gB and gH-gL in the regulation of cell fusion has been explored, whether host factors are directly involved in this regulation process is unknown. Here, we discovered host factors that modulated VZV gB/gH-gL mediated cell fusion via high-throughput screening of bioactive compounds with known cellular targets. Two structurally related non-antibiotic macrolides, tacrolimus and pimecrolimus, both significantly increased VZV gB/gH-gL mediated cell fusion. These compounds form a drug-protein complex with FKBP1A, which binds to calcineurin and specifically inhibits calcineurin phosphatase activity. Inhibition of calcineurin phosphatase activity also enhanced both herpes simplex virus-1 fusion complex and syncytin-1 mediated cell fusion, indicating a broad role of calcineurin in modulating this process. To characterize the role of calcineurin phosphatase activity in VZV gB/gH-gL mediated fusion, a series of biochemical, biological and infectivity assays was performed. Pimecrolimus-induced, enhanced cell fusion was significantly reduced by shRNA knockdown of FKBP1A, further supporting the role of calcineurin phosphatase activity in fusion regulation. Importantly, inhibition of calcineurin phosphatase activity during VZV infection caused exaggerated syncytia formation and suppressed virus propagation, which was consistent with the previously reported phenotypes of gB and gH hyperfusogenic VZV mutants. Seven host cell proteins that remained uniquely phosphorylated when calcineurin phosphatase activity was inhibited were identified as potential downstream factors involved in fusion regulation. These findings demonstrate that calcineurin is a critical host cell factor pivotal in the regulation of VZV induced cell fusion, which is essential for VZV pathogenesis.
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Tsurudome, Masato, Machiko Nishio, Morihiro Ito, Shunsuke Tanahashi, Mitsuo Kawano, Hiroshi Komada, and Yasuhiko Ito. "Effects of Hemagglutinin-Neuraminidase Protein Mutations on Cell-Cell Fusion Mediated by Human Parainfluenza Type 2 Virus." Journal of Virology 82, no. 17 (June 18, 2008): 8283–95. http://dx.doi.org/10.1128/jvi.00460-08.

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ABSTRACT The monoclonal antibody M1-1A, specific for the hemagglutinin-neuraminidase (HN) protein of human parainfluenza type 2 virus (HPIV2), blocks virus-induced cell-cell fusion without affecting the hemagglutinating and neuraminidase activities. F13 is a neutralization escape variant selected with M1-1A and contains amino acid mutations N83Y and M186I in the HN protein, with no mutation in the fusion protein. Intriguingly, F13 exhibits reduced ability to induce cell-cell fusion despite its multistep replication. To investigate the potential role of HPIV2 HN protein in the regulation of cell-cell fusion, we introduced these mutations individually or in combination to the HN protein in the context of recombinant HPIV2. Following infection at a low multiplicity, Vero cells infected with the mutant virus H-83/186, which carried both the N83Y and M186I mutations, remained as nonfused single cells at least for 24 h, whereas most of the cells infected with wild-type virus mediated prominent cell-cell fusion within 24 h. On the other hand, the cells infected with the mutant virus, carrying either the H-83 or H-186 mutation, mediated cell-cell fusion but less efficiently than those infected with wild-type virus. Irrespective of the ability to cause cell-cell fusion, however, every virus could infect all the cells in the culture within 48 h after the initial infection. These results indicated that both the N83Y and M186I mutations in the HN protein are involved in the regulation of cell-cell fusion. Notably, the limited cell-cell fusion by H-83/186 virus was greatly promoted by lysophosphatidic acid, a stimulator of the Ras and Rho family GTPases.
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Dissertations / Theses on the topic "Virus Cell Fusion"

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Barkley, Russell. "Investigation of an Oncolytic MeV Cell-Cell Fusion Phenomenon Induced by an siRNA." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/41531.

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Oncolytic measles virus is a promising cancer therapeutic in clinical trials which possesses multiple characteristics that are advantageous over traditional therapies. Currently, clinical oncolytic measles virus vectors are unmodified or express reporter transgenes that benefit its therapeutic efficacy. The next phase in its development will see genetically engineered vectors encoding transgenes that enhance its antineoplastic effects. To this end, preclinical research has focused on studying novel transgenes which favour viral replication, cytotoxicity, and the anti-cancer immune response. We sought to encode artificial micoRNAs targeting RIG-I as a strategy to interfere with innate immunity. Silencing RIG-I with multiple siRNAs yielded one which promotes measles virus syncytia formation through a mechanism that appears to be independent of RIG-I. The mechanism caused by the siRNA leads to enhanced measles virus cell-cell fusion and has peculiar characteristics which are not fully understood.
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Garg, Himanshu. "Feline Immunodeficiency Virus (FIV) Envelope Glycoprotein-Mediated Cell Fusion and Apoptosis." NCSU, 2003. http://www.lib.ncsu.edu/theses/available/etd-11042003-141554/.

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Feline Immunodeficiency Virus (FIV) and Human Immunodeficiency Virus (HIV) are lentiviruses that are remarkable similar in their genomic organization, receptor usage and pathogenesis. Based on this FIV has evolved into a well-established small animal model for studying AIDS. FIV and HIV cause a progressive depletion of T cells via a still unknown mechanism though numerous studies support a role of membrane expressed HIV env glycoprotein in apoptotic killing of CD4+ T cells. HIV env glycoprotein is a heterodimer of surface expressed gp120 that binds to CD4 and a chemokine receptor and transmembrane gp41 that mediates fusion and syncytia formation. The role of the fusion process in HIV env-mediated apoptosis remains controversial even though evidence suggests that cytopathic effect of HIV is related to the fusogenic potential of env glycoprotein. Blocking HIV env receptor interactions either at the level of gp120 or gp41 blocks both syncytia formation and apoptosis. This suggests a crucial role for HIV gp41 in fusion, as well as apoptosis. The hydrophobic pre-transmembrane (pre-TM) region of HIV gp41 is important for membrane fusion and sequence analysis reveals a similar region in FIV gp41. The current study was undertaken to determine the role of different regions of FIV env in mediating fusion and apoptosis in bystander cells and to determine whether the two phenomena are related. FIV env interactions with target cells were blocked at the level of gp120 or gp41 and the effect of these on fusion and apoptosis studied. The role of FIV gp41 pre-TM region in fusion and apoptosis was also determined. Our findings support a role of FIV env in apoptotic loss of T cells and this phenomenon correlates with env-mediated fusion.
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Bickerton, Erica Jane. "Cellular tropism and cell-to-cell fusion properties of the infectious bronchitis virus spike glycoprotein." Thesis, University of Warwick, 2010. http://wrap.warwick.ac.uk/35165/.

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There are numerous vaccines available for the control of infectious bronchitis virus (IBV) in poultry, however protection is short-lived and poorly cross-protective between strains. The vaccines must currently be grown in embryonated eggs, a cumbersome and expensive process. The ability to grow vaccines on a cell-line such as Vero cells would be highly advantageous. The spike (S) glycoprotein of IBV is comprised of two subunits, S1 and S2, has a vital role in virulence in vivo and is responsible for cellular tropism in vitro. This project aims to identify the amino acids present in the S glycoprotein involved in determination of cellular tropism and cell-to-cell fusion. The IBV Beaudette strain is able to replicate in both primary chick kidney (CK) cells and Vero cells, whereas the IBV M41 strain replicates in primary cells only. Recombinant IBVs with chimaeric S genes were generated using a reverse genetics system with the genomic background of Beaudette and part of the S gene from M41. Their growth characteristics and cellular tropism were investigated. The S2 subunit of Beaudette was found to be sufficient to confer the ability to grow on Vero cells and swapping just three amino acids with corresponding ones from M41 was sufficient to remove the ability of the Beaudette S glycoprotein for growth on Vero cells. Beaudette was further adapted to syncytia formation on Vero cells by serial passage and isolates were sequenced to identify amino acid changes between parent and Vero-adapted viruses that are potentially involved in cell-to-cell fusion. Understanding the way in which IBV infects host cells is vital in order to rationally design better vaccination and treatment strategies and help to reduce the prevalence of IBV infection in poultry worldwide. Using the IBV reverse genetics system, we now have the potential to grow IBV vaccines on Vero cells.
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Symeonides, Menelaos. "HIV-1-Induced Cell-Cell Fusion: Host Regulation And Consequences For Viral Spread." ScholarWorks @ UVM, 2016. https://scholarworks.uvm.edu/graddis/589.

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Human immunodeficiency virus type 1 (HIV-1) is a human retrovirus of the lentivirus subgroup which primarily infects T cells and macrophages, and causes acquired immune deficiency syndrome (AIDS). Since its emergence in the early 1980s, HIV-1 has caused a global pandemic which is still responsible for over one million deaths per year, primarily in sub-Saharan Africa. HIV-1 has been the subject of intense study for over three decades, which has resulted not only in major advances in cell biology, but also in numerous drug treatments that effectively control the infection. However, cessation of treatment always results in reemergence of the infection due to the ability of HIV-1 (and other lentiviruses) to establish a persistent quiescent infection known as latency. The elimination of latently-infected cells is the primary goal of current research towards a cure for HIV-1, alongside efforts to develop vaccines, which have thus far been fruitless. The spread of HIV-1 to susceptible target cells (which express the receptor CD4 and a co-receptor; CXCR4 or CCR5) can take place when antigen-presenting cells, such as dendritic cells, capture virus particles and then pass them on to target cells, without themselves becoming infected. Alternatively, productively infected T cells or macrophages can spread HIV-1 either by shedding virus particles to the milieu, which are then stochastically acquired by target cells, or through transient contacts between infected and uninfected cells known as virological synapses (VSs). VS-mediated cell-to-cell transmission is thought to be highly efficient due to the release of virus directly onto (or very near to) a target cell, and some evidence suggests that the VS is a privileged site which allows the virus to evade neutralizing antibodies and drugs. However, and most importantly, it is of central interest to us because the same transient cell adhesions that facilitate virus transfer can also result in the fusion of the two cells to form a syncytium, due to the presence of the viral fusogen Env and its receptor and co-receptor on either side of the VS. While T cell syncytia can be found in vivo, they remain small, and it appears that the majority of VSs resolve without fusion. The regulation of HIV-1-induced cell-cell fusion and the fate of those syncytia are the focus of the work presented here. A family of host transmembrane proteins, the tetraspanins, which regulate cell-cell fusion in other contexts (e.g. the fusion of myoblasts to form and maintain myotubes), were found to inhibit HIV-1-induced cell-cell fusion. Our investigations have further characterized this regulation, concluding that tetraspanins allow cells to reach the fusion intermediate known as hemifusion before their ability to repress fusion takes effect. In parallel, because syncytia are nevertheless found both in infected individuals and in a humanized mouse model for HIV-1, we also became interested in whether small T cell-based syncytia were able to participate in HIV-1 spread by transmitting virus to target cells. Using a simple three dimensional in vitro culture system which closely recapitulates those in situ observations, we found that small syncytia can contact target cells and transmit virus without fusing with them. Overall, these studies further our understanding of HIV-1-induced syncytia and reveal a previously unrecognized role for these entities as active participants in HIV-1 spread.
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Leung, Sze-Yui Horasis, and 梁思睿. "Fibronectin: role in viral cell association, fusion and entry of influenza A virus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B48329708.

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The influenza A viral hemagglutinin (HA) protein binds to sialic acid (SA) groups of cellular surface glycoproteins to achieve viral attachment and entry. The SA binding specificity of HA is one of the major determinants for controlling viral tropism and host specificity. Fibronectin (FN) is a ubiquitinious glycoprotein secreted on cell surface, either circulating in plasma, or as one of the best characterized components of the extra cellular matrix. With its binding properties towards different types of molecules and pathogens, it has been utilized by different bacterial and viral pathogens for binding, entry, propagation and pathogenesis. The binding affinity and region of plasma FN to influenza A viral glycoprotein was identified in early 1980s. Evidence also suggests the binding is SA associated. FN associates with different viral pathogens. However, evidence of FN direct involvement in influenza A pathogenesis remains unknown. The objective of this thesis is to test the involvement of cellular FN in influenza A viral infection. To perform the study, FN siRNA and anti-FN antibody were applied. This study demonstrated possible involvement of FN in the replication of human H1N1 and highly pathogenic avian H5N1 viruses. It also discovered that FN is very important for the replication of H1N1 virus, but not H5N1 virus. Interestingly, the result suggested that FN does not affect the initial virus-host binding, but it has an effect on post-attachment events. Key amino acid positions controlling the SA binding specificity of seasonal human or avian influenza A viruses have been identified in the HA. In this thesis, reverse genetics and mutagenic work identified that viruses with a α2,3-linked SA (SA α2,3) binding preference were not inhibited by anti-FN antibody, while viruses with a α2,6-linked SA (SA α2,6) specificity were severely inhibited. This surprising finding of SA binding preference related FN involvement in post-attachment event led to the further investigation on the structural involvement of FN and viral entry pathway analysis. The 9th and 10th of type III repeating units of FN form the cell-binding domain of the protein for cell attachment. From site specific antibody inhibitory studies, the cell binding region of FN near the synergy adhesion site(SAS) and Arg-Gly-Asp-Ser(RGDS) cell adhesion signal was identified to be important for the replication of viruses that have a α2,6 SA binding preference, but it was also found to be independent of α5β1 integrin receptor. After attaching to a host cell, the virus was internalized in an endosome via clathrin- or caveolin- mediated endocytosis. By application of pathway inhibitors, the FN association with viral entry pathway was evaluated. Though this study failed to identify a single specific FN mediated viral entry pathway, this pathway study indicated the possibility of FN various involvement in influenza viral entry. The study indeed indicated that viruses have difference SA binding preferences are different in their choices in viral entry pathways. This thesis did not only introduce cellular FN as a novel host factor, but also identified possible target and brought new light in the control of influenza A viral infection.
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Wagenaar, Timothy Robert. "Regulation of infected cell fusion by the vaccinia virus A56 and K2 proteins." College Park, Md.: University of Maryland, 2008. http://hdl.handle.net/1903/8044.

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Thesis (Ph. D.) -- University of Maryland, College Park, 2008.
Thesis research directed by: Dept. of Cell Biology & Molecular Genetics. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
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Hummel, Kimberly Brown. "Alteration of the measles virus glycoproteins as a mechanism to reduce cell fusion during persistence." Diss., Georgia Institute of Technology, 1994. http://hdl.handle.net/1853/25597.

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Hutchinson, Lloyd M. "Glycoprotein K of herpes simplex virus (HSV), role in viral egress and HSV-induced cell-cell fusion." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0016/NQ30094.pdf.

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Al-Torki, Reem. "Mapping of B-cell epitopes on the fusion protein of human respiratory syncytial virus." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415976.

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Marques, Sandra Eugénia Leite. "Expressão em Escherichia coli de antigénios do Cell fusing agent virus (Flaviviridae: Flavivirus) como proteína de fusão." Master's thesis, Faculdade de Ciências Médicas. UNL, 2012. http://hdl.handle.net/10362/8531.

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RESUMO: O Cell Fusing Agent Vírus (CFAV), considerado como o primeiro “flavivírus específicos de insectos” (ISF), parece estar exclusivamente adaptado aos seus hospedeiros, não replicando em células de vertebrados. Apesar de ter sido identificado há mais de três décadas (1975), a verdade é que muito pouco se conhece sobre a sua biologia. Dado o seu parentesco filogenético com alguns outros flavivírus encontrados naturalmente em mosquitos de diferentes géneros colhidos em diferentes regiões do globo, este vírus poderá ser usado como modelo para o estudo de ISF. No entanto, necessitam do desenvolvimento de ferramentas básicas, tais como clones moleculares ou baterias de soros contendo anticorpos que reconheçam uma ou mais proteínas codificadas pelo genoma viral, produzidas, por exemplo, a partir de antigénios virais produzidos de forma recombinante. Com este trabalho pretendeu-se a optimização de protocolos que permitiram a expressão e purificação parcial de quatro proteínas [duas proteínas estruturais (C e E) e duas não estruturais (NS3hel e NS5B)] do CFAV em E. coli, todas elas produzidas como proteínas de fusão com “caudas” (tags) de hexahistidina nos seus extremos carboxilo. Para a expansão do CFAV foram utilizadas células Aedes albopictus (C6/36). Após a realização da extracção do RNA viral e a obtenção de cDNA, procedeu-se amplificação, por RT-PCR, das regiões codificantes das proteínas C, E, NS3hel e NS5B, utilizando primers específicos. Os quatro fragmentos de DNA foram independentemente inseridos no vector pJTE1.2/blunt usando E. coli NovaBlue como hospedeira de clonagem e, posteriormente, inseridos em vectores de expressão pET-28b e pET-29b usando E. coli BL21(DE3)pLysS e Rosetta(DE3)pLysS como hospedeiras de expressão. Após da indução, expressão e purificação das proteínas recombinantes C, E, NS3hel e NS5B, foi confirmada a autenticidade destas proteínas produzidas através do método Western Blot com um anticorpo anti-histidina. --------- ABSTRACT: The Cell Fusing Agent virus (CFAV) considered as the first "insect- specific flavivirus" (ISF) and seems to be uniquely adapted to their hosts, not replicating in vertebrate cells. Although it has been known for more than three decades (1975), the truth is very little is known about its biology. Given its close phylogenetic relationship with other flavivirus naturally circulating in various genera of mosquitoes collected from different regions of the globe, this virus could be used as a model for the study of ISF. However, such studies require the development of experimental basic tools, such as molecular clones or serum batteries containing antibodies that recognize one or more proteins encoded by the viral genome, produced, for example, from viral antigens recombinant produced. In this work, we carried out the optimization of protocols that allowed the expression and partial purification of four proteins [two structural proteins (C and E) and two nonstructural proteins (NS3hel and NS5B)] CFAV in E. coli as fusion protein for c-terminal hexahistidine tags. For the expansion of the CFAV we used Aedes albopictus (C6/36) cells. After completion of the viral RNA extraction and cDNA obtained, amplification of the coding regions of the C, E, NS5B and NS3hel proteins was carried out by RT-PCR using specific primers. The four DNA fragments were independently inserted into the vector pJTE1.2/blunt using E. coli NovaBlue as cloning host and then inserted into expression vectors pET-28b and pET-29b using E. coli BL21(DE3)pLysS and Rosetta(DE3)pLysS as expression host. After induction, expression and purification of recombinant C, E, NS3hel and NS5B proteins Western Blot analyses with an anti-histidine antibody confirmed the authenticity of these proteins produced.
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Book chapters on the topic "Virus Cell Fusion"

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Spear, Patricia G. "Virus-Induced Cell Fusion." In Cell Fusion, 3–32. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4757-9598-1_1.

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Weed, Darin J., and Anthony V. Nicola. "Herpes simplex virus Membrane Fusion." In Cell Biology of Herpes Viruses, 29–47. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-53168-7_2.

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Yeagle, Philip L., Daniel R. Kelsey, Thomas D. Flanagan, and Joyce Young. "Inhibition of Sendai Virus Fusion and Phospholipid Vesicle Fusion: Implications for the Pathway of Membrane Fusion." In Cell and Model Membrane Interactions, 163–77. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4615-3854-7_10.

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Bossart, Katharine N., and Christopher C. Broder. "Viral Glycoprotein-Mediated Cell Fusion Assays Using Vaccinia Virus Vectors." In Vaccinia Virus and Poxvirology, 309–31. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1385/1-59259-789-0:309.

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Lanzrein, Markus, Magda Spycher-Burger, and Christoph Kempf. "Semliki Forest Virus Induced Cell-Cell Fusion and Pore Formation." In Biological Membranes: Structure, Biogenesis and Dynamics, 341–48. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78846-8_34.

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Loyter, A., M. Tomasi, A. G. Gitman, L. Etinger, and O. Nussbaum. "The Use of Specific Antibodies to Mediate Fusion Between Sendai Virus Envelopes and Living Cells." In Ciba Foundation Symposium 103 - Cell Fusion, 163–80. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720844.ch11.

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Koblet, H., A. Omar, U. Kohler, and Ch Kempf. "Investigation of Cell-Cell Fusion in Semliki Forest Virus (SFV) Infected C6/36 (Mosquito) Cells." In Invertebrate and Fish Tissue Culture, 140–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73626-1_34.

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Yoshida, Keiichi, Natsuko Kawano, Yuichiroh Harada, and Kenji Miyado. "Role of CD9 in Sperm–Egg Fusion and Virus-Induced Cell Fusion in Mammals." In Sexual Reproduction in Animals and Plants, 383–91. Tokyo: Springer Japan, 2014. http://dx.doi.org/10.1007/978-4-431-54589-7_31.

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Yi, Yanjie, Anjali Singh, Joanne Cutilli, and Ronald G. Collman. "Use of Dual Recombinant Vaccinia Virus Vectors to Assay Viral Glycoprotein-Mediated Fusion with Transfection-Resistant Primary Cell Targets." In Vaccinia Virus and Poxvirology, 333–46. Totowa, NJ: Humana Press, 2004. http://dx.doi.org/10.1385/1-59259-789-0:333.

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Nash, Therese C., Thomas M. Gallagher, and Michael J. Buchmeier. "MHVR-Independent Cell-Cell Spread of Mouse Hepatitis Virus Infection Requires Neutral pH Fusion." In Advances in Experimental Medicine and Biology, 351–57. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1899-0_57.

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Conference papers on the topic "Virus Cell Fusion"

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Aranda, S., and H. Aranda-Espinoza. "Virus—Cell—Fusion." In MEDICAL PHYSICS. ASCE, 1998. http://dx.doi.org/10.1063/1.56373.

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LeDuc, Philip R., and Michael J. Betenbaugh. "Implementation of a Pharmocokinetic Approach to a Baculovirus System for Analytic Solutions to Virus and Cell Interactions." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0282.

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Abstract The baculovirus, Autographa californica multiple nuclear polyhedrosis virus (AcMNPV), expression system can be employed for a variety of different cellular applications. In recent years, this baculovirus system has been manipulated to serve as a recombinant system for the expression of heterologous proteins and as a possible retrovirus for gene therapy. A quantitative understanding of the cellular mechanics of virus trafficking would be useful in developing viral expression systems, understanding gene therapy and maximizing recombinant protein production. An analytic solution is presented which incorporates a pharmocokinetic system in order to analyze this problem of viral and cellular mechanics. The multiple stages of viral infection systems, specifically for the baculovirus system, include attachment, internalization, endosomal fusion, cytosol transportation, and nuclear accumulation. The effects of the rate parameters are investigated to determine the parameter sensitivity of the viral infection model in relation to accumulation of surface virus, internalized virus and nuclear virus. The concepts from this model can be used to design infection regimens for various cell lines and to analyze the inherent inefficiency of current baculovirus infecting systems. This approach can also be used to determine the effects of the rate-limiting behaviors exhibited by these types of cellular mechanics and can be further implemented to examine other types of infection applications including viral gene therapy [1].
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Gheysen, D., L. Piérard, P. Jacobs, H. R. Lijnen, A. Bollen, and D. Collen. "PROPERTIES OF A HUMAN RECOMBINANT FUSION PROTEIN OF THE ‘FINGER’ DOMAIN OF TISSUE-TYPE PLASMINOGEN ACTIVATOR (t-PA) AND A TRUNCATED SINGLE CHAIN UROKINASE-TYPE PLASMINOGEN ACTIVATOR (scu-PA)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643941.

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A hybrid between human tissue-type plasminogen activator (t-PA) and human single chain urokinase-type plasminogen activator (scu-PA) was obtained by ligation of cDNA fragments encoding the NH2-terminal amino acids 1 to 67 of t-PA and the COOH-ter-minal amino acids 136 to 411, of scu-PA. Both this chimaeric cDNA and cDNA encoding scu-PA were expressed in a mammalian system (HAK-cells) using bovine papilloma virus (BPV) derived vectors. Two stable cell lines were obtained which secreted the recombinant hybrid and the scu-PA at 1 μg/ml and 2 μg/ml u-PA related antigen respectively into the culture medium. Following purification by Zinc chelate Sepharose, immunoadsorption chromatography, benzamidine-Sepharose and Ultrogel AcA44 gel filtration, highly purified proteins were obtained with a yield of about 200 μg/1. SDS gel electrophoresis under reducing conditions showed single bands with M 43,000 and M 50,000 respectively. Following conversion to urokinase with plasmin, both proteins had a specific amidolytic activity comparable to that of natural scu-PA. Both proteins activated plasminogen directly with km1.4 and 0.5 μM and k2 0.0034 s and 0.0027 s . Neither protein bound specifically to fibrin.Thus the fusion of the finger-like domain of t-PA to the COOH-terminal part of scu-PA does not confer fibrin affinity of t-PA to this chimaeric protein. However, peptide material can be fused to the COOH-terminal part of scu-PA without perturbing its enzymatic properties.
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Furihata, Kenichi, Diane J. Nugent, Amy L. Bissonette, Elizabeth Vokac, and Thomas J. Kunicki. "PRODUCTION OF HUMAN MONOCLONAL ANTIBODIESSPECIFIC FOR PLATELET MEMBRANE GLYCOPROTEIN IIIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643705.

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Human monoclonal antibodies specific for platelet membrane glycoproteins (GPs) arepotentially important reagentsfor studies of the immunogenicity of membrane glycoproteins. A human monoclonalautoantibody, 5E5, reactive with plateletGPIIIa has been developed (Nugent, et al.,Blood, 1987, in press). In this report, we describe the production of additional human monoclonal antibodies specific for GPIIIa. Peripheral blood lymphocytes fromone patient with post-transfusion purpur(PTP) and one woman who had delivered an infant with neonatal alloimmune thrombocytopenic purpura (NATP) were used as a source of antigen-specific lymphocytes. A B-lympho-cyte-enriched population was transformed with Epstein Barr virus, strain B95-8, and cultured in microtiter plates. After two weeks, culture supernatants were screened by an antigen-capture ELISA wherein murine monoclonal antibody specificfor the GPIIb-IIIa complex was used to holdcorresponding antigen from a lysate ofnormal platelets. B-lymphoblastoid cell lines producing IgG and/or IgM antibodies were expanded and either cloned by limiting dilution technqiue or hybridized with a HAT-sensitive, ouabain-resistant heterohybrid fusion line, F6, using polyethylene glycol. Hybridomas were selected in medium containing HAT andouabain. After twoweeks, hybridomas producing anti-GPIIb and/or anti-GPIIIa antibody were cloned by limiting dilution. Culture supernatants from cloned B-lymphoblastoid cell lines and cloned hybridomas were rescreened by ELISA wherein affinity-purified GPIIIa or other platelet GP weredirectly conjugatedto microtiter plates. One IgM antibody produced by acloned B-lymphoblastoid cellline (CH16) andtwo IgG antibodies produced bycloned hybridomas(Del5.19 and Del5.23) were shownto react with GPIIIa but not other GP. Further characterization of these human monoclonal antibodies, produced continuouslyin culture now for four months, is in progress.
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Clarke, C. J., V. Solodushko, and B. W. Fouty. "Fusing the Ectodomain of the Respiratory Syncytial Virus Protein F to Proteins Can Transfer Them to Other Cells." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a3976.

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Reports on the topic "Virus Cell Fusion"

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Gafny, Ron, A. L. N. Rao, and Edna Tanne. Etiology of the Rugose Wood Disease of Grapevine and Molecular Study of the Associated Trichoviruses. United States Department of Agriculture, September 2000. http://dx.doi.org/10.32747/2000.7575269.bard.

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Rugose wood is a complex disease of grapevines, characterized by modification of the woody cylinder of affected vines. The control of rugose wood is based on the production of healthy propagation material. Detection of rugose wood in grapevines is difficult and expensive: budwood from tested plants is grafted onto sensitive Vitis indicators and the appearance of symptoms is monitored for 3 years. The etiology of rugose wood is complex and has not yet been elucidated. Several elongated clostero-like viruses are consistently found in affected vines; one of them, grapevine virus A (GVA), is closely associated with Kober stem grooving, a component of the rugose wood complex. GVA has a single-stranded RNA genome of 7349 nucleotides, excluding a polyA tail at the 3' terminus. The GVA genome includes five open reading frames (ORFs 1-5). ORF 4, which encodes for the coat protein of GVA, is the only ORF for which the function was determined experimentally. The original objectives of this research were: 1- To produce antisera to the structural and non-structural proteins of GVA and GVB and to use these antibodies to establish an effective detection method. 2- Develop full length infectious cDNA clones of GVA and GVB. 3- Study the roll of GVA and GVB in the etiology of the grapevine rugose wood disease. 4- Determine the function of Trichovirus (now called Vitivirus) encoded genes in the virus life cycle. Each of the ORFs 2, 3, 4 and 5 genes of GVA were cloned and expressed in E. coli and used to produce antisera. Both the CP (ORF 4) and the putative MP (ORF 3) were detected with their corresponding antisera in-GVA infected N. benthamiana and grapevine. The MP was first detected at an early stage of the infection, 6-12 h after inoculation, and the CP 2-3 days after inoculation. The MP could be detected in GVA-infected grapevines that tested negative for CP, both with CP antiserum and with a commercially available ELISA kit. Antisera to ORF 2 and 5 encoded proteins could react with the recombinant proteins but failed to detect both proteins in GVA infected plants. A full-length cDNA clone of grapevine virus A (GVA) was constructed downstream from the bacteriophage T7 RNA polymerase promoter. Capped in vitro transcribed RNA was infectious in N. benthamiana and N. clevelandii plants. Symptoms induced by the RNA transcripts or by the parental virus were indistinguishable. The infectivity of the in vitro-transcribed RNA was confirmed by serological detection of the virus coat and movement proteins and by observation of virions by electron microscopy. The full-length clone was modified to include a gus reporter gene and gus activity was detected in inoculated and systemic leaves of infected plants. Studies of GVA mutants suggests that the coat protein (ORF 4) is essential for cell to cell movement, the putative movement protein (ORF 3) indeed functions as a movement protein and that ORF 2 is not required for virus replication, cell to cell or systemic movement. Attempts to infect grapevines by in-vitro transcripts, by inoculation of cDNA construct in which the virus is derived by the CaMV 35S promoter or by approach grafting with infected N. benthamiana, have so far failed. Studies of the subcellular distribution of GFP fusion with each of ORF 2, 3 and 4 encoded protein showed that the CP fusion protein accumulated as a soluble cytoplasmatic protein. The ORF 2 fusion protein accumulated in cytoplasmatic aggregates. The MP-GFP fusion protein accumulated in a large number of small aggregates in the cytoplasm and could not move from cell to cell. However, in conditions that allowed movement of the fusion protein from cell to cell (expression by a PVX vector or in young immature leaves) the protein did not form cytoplasmatic aggregates but accumulated in the plasmodesmata.
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Epel, Bernard L., Roger N. Beachy, A. Katz, G. Kotlinzky, M. Erlanger, A. Yahalom, M. Erlanger, and J. Szecsi. Isolation and Characterization of Plasmodesmata Components by Association with Tobacco Mosaic Virus Movement Proteins Fused with the Green Fluorescent Protein from Aequorea victoria. United States Department of Agriculture, September 1999. http://dx.doi.org/10.32747/1999.7573996.bard.

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The coordination and regulation of growth and development in multicellular organisms is dependent, in part, on the controlled short and long-distance transport of signaling molecule: In plants, symplastic communication is provided by trans-wall co-axial membranous tunnels termed plasmodesmata (Pd). Plant viruses spread cell-to-cell by altering Pd. This movement scenario necessitates a targeting mechanism that delivers the virus to a Pd and a transport mechanism to move the virion or viral nucleic acid through the Pd channel. The identity of host proteins with which MP interacts, the mechanism of the targeting of the MP to the Pd and biochemical information on how Pd are alter are questions which have been dealt with during this BARD project. The research objectives of the two labs were to continue their biochemical, cellular and molecular studies of Pd composition and function by employing infectious modified clones of TMV in which MP is fused with GFP. We examined Pd composition, and studied the intra- and intercellular targeting mechanism of MP during the infection cycle. Most of the goals we set for ourselves were met. The Israeli PI and collaborators (Oparka et al., 1999) demonstrated that Pd permeability is under developmental control, that Pd in sink tissues indiscriminately traffic proteins of sizes of up to 50 kDa and that during the sink to source transition there is a substantial decrease in Pd permeability. It was shown that companion cells in source phloem tissue export proteins which traffic in phloem and which unload in sink tissue and move cell to cell. The TAU group employing MP:GFP as a fluorescence probe for optimized the procedure for Pd isolation. At least two proteins kinases found to be associated with Pd isolated from source leaves of N. benthamiana, one being a calcium dependent protein kinase. A number of proteins were microsequenced and identified. Polyclonal antibodies were generated against proteins in a purified Pd fraction. A T-7 phage display library was created and used to "biopan" for Pd genes using these antibodies. Selected isolates are being sequenced. The TAU group also examined whether the subcellular targeting of MP:GFP was dependent on processes that occurred only in the presence of the virus or whether targeting was a property indigenous to MP. Mutant non-functional movement proteins were also employed to study partial reactions. Subcellular targeting and movement were shown to be properties indigenous to MP and that these processes do not require other viral elements. The data also suggest post-translational modification of MP is required before the MP can move cell to cell. The USA group monitored the development of the infection and local movement of TMV in N. benthamiana, using viral constructs expressing GFP either fused to the MP of TMV or expressing GFP as a free protein. The fusion protein and/or the free GFP were expressed from either the movement protein subgenomic promoter or from the subgenomic promoter of the coat protein. Observations supported the hypothesis that expression from the cp sgp is regulated differently than expression from the mp sgp (Szecsi et al., 1999). Using immunocytochemistry and electron microscopy, it was determined that paired wall-appressed bodies behind the leading edge of the fluorescent ring induced by TMV-(mp)-MP:GFP contain MP:GFP and the viral replicase. These data suggest that viral spread may be a consequence of the replication process. Observation point out that expression of proteins from the mp sgp is temporary regulated, and degradation of the proteins occurs rapidly or more slowly, depending on protein stability. It is suggested that the MP contains an external degradation signal that contributes to rapid degradation of the protein even if expressed from the constitutive cp sgp. Experiments conducted to determine whether the degradation of GFP and MP:GFP was regulated at the protein or RNA level, indicated that regulation was at the protein level. RNA accumulation in infected protoplast was not always in correlation with protein accumulation, indicating that other mechanisms together with RNA production determine the final intensity and stability of the fluorescent proteins.
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