Relevant bibliographies by topics / Viral proteins

Contents

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

Academic literature on the topic 'Viral proteins'

Author: Grafiati
Published: 4 June 2021
Last updated: 30 July 2024

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Journal articles on the topic "Viral proteins"

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Flint, Jane, and Thomas Shenk. "VIRAL TRANSACTIVATING PROTEINS." Annual Review of Genetics 31, no. 1 (December 1997): 177–212. http://dx.doi.org/10.1146/annurev.genet.31.1.177.

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Fischer, Wolfgang B., Gerhard Thiel, and Rainer H. A. Fink. "Viral membrane proteins." European Biophysics Journal 39, no. 7 (August 12, 2009): 1041–42. http://dx.doi.org/10.1007/s00249-009-0525-y.

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Seet, Bruce T., and Grant McFadden. "Viral chemokine‐binding proteins." Journal of Leukocyte Biology 72, no. 1 (July 2002): 24–34. http://dx.doi.org/10.1189/jlb.72.1.24.

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Verdaguer, Nuria, Diego Ferrero, and Mathur R. N. Murthy. "Viruses and viral proteins." IUCrJ 1, no. 6 (October 14, 2014): 492–504. http://dx.doi.org/10.1107/s205225251402003x.

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For more than 30 years X-ray crystallography has been by far the most powerful approach for determining the structures of viruses and viral proteins at atomic resolution. The information provided by these structures, which covers many important aspects of the viral life cycle such as cell-receptor recognition, viral entry, nucleic acid transfer and genome replication, has extensively enriched our vision of the virus world. Many of the structures available correspond to potential targets for antiviral drugs against important human pathogens. This article provides an overview of the current knowledge of different structural aspects of the above-mentioned processes.
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Rosengard, Ariella M., and Joseph M. Ahearn. "Viral complement regulatory proteins." Immunopharmacology 42, no. 1-3 (May 1999): 99–106. http://dx.doi.org/10.1016/s0162-3109(99)00012-0.

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Lee, Hyun-Cheol, Kiramage Chathuranga, and Jong-Soo Lee. "Intracellular sensing of viral genomes and viral evasion." Experimental & Molecular Medicine 51, no. 12 (December 2019): 1–13. http://dx.doi.org/10.1038/s12276-019-0299-y.

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AbstractDuring viral infection, virus-derived cytosolic nucleic acids are recognized by host intracellular specific sensors. The efficacy of this recognition system is crucial for triggering innate host defenses, which then stimulate more specific adaptive immune responses against the virus. Recent studies show that signal transduction pathways activated by sensing proteins are positively or negatively regulated by many modulators to maintain host immune homeostasis. However, viruses have evolved several strategies to counteract/evade host immune reactions. These systems involve viral proteins that interact with host sensor proteins and prevent them from detecting the viral genome or from initiating immune signaling. In this review, we discuss key regulators of cytosolic sensor proteins and viral proteins based on experimental evidence.
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Watson, Alastair, Maximillian J. S. Phipps, Howard W. Clark, Chris-Kriton Skylaris, and Jens Madsen. "Surfactant Proteins A and D: Trimerized Innate Immunity Proteins with an Affinity for Viral Fusion Proteins." Journal of Innate Immunity 11, no. 1 (October 5, 2018): 13–28. http://dx.doi.org/10.1159/000492974.

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Innate recognition of viruses is an essential part of the immune response to viral pathogens. This is integral to the maintenance of healthy lungs, which are free from infection and efficient at gaseous exchange. An important component of innate immunity for identifying viruses is the family of C-type collagen-containing lectins, also known as collectins. These secreted, soluble proteins are pattern recognition receptors (PRRs) which recognise pathogen-associated molecular patterns (PAMPs), including viral glycoproteins. These innate immune proteins are composed of trimerized units which oligomerise into higher-order structures and facilitate the clearance of viral pathogens through multiple mechanisms. Similarly, many viral surface proteins form trimeric configurations, despite not showing primary protein sequence similarities across the virus classes and families to which they belong. In this review, we discuss the role of the lung collectins, i.e., surfactant proteins A and D (SP-A and SP-D) in viral recognition. We focus particularly on the structural similarity and complementarity of these trimeric collectins with the trimeric viral fusion proteins with which, we hypothesise, they have elegantly co-evolved. Recombinant versions of these innate immune proteins may have therapeutic potential in a range of infectious and inflammatory lung diseases including anti-viral therapeutics.
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Shalitin, Dror, and Shmuel Wolf. "Interaction between phloem proteins and viral movement proteins." Functional Plant Biology 27, no. 9 (2000): 801. http://dx.doi.org/10.1071/pp99153.

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This paper originates from a presentation at the International Conference on Assimilate Transport and Partitioning, Newcastle, NSW, August 1999 Recent studies support the concept that long-distance signals are involved in the regulation of resource allocation among the various plant organs. Following the finding that viral movement proteins (MPs) can exert an effect on sugar metabolism and resource allocation at sites distant from their expression, we suggested that the MPs interfere with an element(s) involved in the plant’s endogenous long-distance signal network. To provide experimental support for this hypothesis, several unique procedures were employed to identify interactions between viral MPs and phloem sap proteins (PSPs) collected from cut petioles of squash (Cucurbita pepo L. subsp. pepo) and melon (Cucumis melo L.) plants. Far-western experiments with blotted PSPs, using both bacteria-overexpressed and in vitro-translated CMV- and TMV-MPs, revealed that the two virally encoded proteins react specifically with more than one PSP. Moreover, isolation of the naturally folded phloem protein in an affinity column containing a TMV-MP-maltose-binding protein indicated, once again, an interaction between the viral protein and similar PSPs. Two melon PSPs with molecular masses of 8 and 23 kDa were found to specifically interact with both the CMV- and TMV-MPs. The possible effects of this interaction in terms of altering the process of phloem transport and resource allocation are discussed.
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Zhilinskaya, I. N. "Mimicry between respiratory virus proteins and some human immune proteins." Russian Journal of Infection and Immunity 10, no. 2 (May 22, 2020): 305–14. http://dx.doi.org/10.15789/2220-7619-mbr-1179.

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A comparative analysis on search for amino acid sequences in viral proteins causing respiratory infections (or respiratory infections syndrome) homologous to amino acid sequences from some human immune proteins was performed. The following viruses were used for comparative computer analysis: coronavirus (SARS-CoV), serotype C subgroup adenovirus C (adenoid 71 strain), measles virus (ICHINOSE-BA strain), rubella (Therien strain) and respiratory syncytial (B1 strain) virus. The search for homologous sequences in viral and human immune proteins was carried out by computer comparison of 12 amino acid fragments, which were assigned as homologous at identity in ≥ 8 positions. The data obtained showed that viral proteins contained homologous motifs in several host immune proteins involved in regulating both the inflammatory response and immune response. Mechanistically, all viruses studied were characterized by sequences homologous to host immune proteins such as complement system proteins, integrins, apoptosis inhibitory proteins, interleukins, and toll-like receptors. Such cellular proteins are actively involved in regulating host inflammatory process and immune response formation. Upon that, a set of host immune proteins, to which homologous fragments were found in viral proteins, was individual for each virus. Interestingly, the largest amount of homologous fragments (up to 20) was mainly concentrated in viral proteins with polymerase and protease activity suggesting that these proteins apart to their major role were involved in production of viral nucleic acids and might participate in regulating host immune system. Envelope, internal and non-structural viral proteins, homologous fragments were detected in much smaller quantities (from 1 to 4). In addition, two fragments homologous to various motifs of the same cellular protein were detected in some viral proteins. Thus, the data obtained further support our understanding that signs of immune system disorders in viral infections can result from multi-layered processes associated with modulation of host innate and adaptive immune system, and open up new approaches to study interaction of viruses with host immune system and identify new functions of viral proteins.
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Chen, Jidang, and Hinh Ly. "Immunosuppression by viral N proteins." Oncotarget 8, no. 31 (June 22, 2017): 50331–32. http://dx.doi.org/10.18632/oncotarget.18597.

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Dissertations / Theses on the topic "Viral proteins"

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Oliveira, Vivian Leite. "Impact of viral mmunomodulatory proteins." Doctoral thesis, Universidade Nova de Lisboa. Instituto de Tecnologia Química e Biológica, 2013. http://hdl.handle.net/10362/11946.

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Dissertation presented to obtain the Ph.D degree in Biology
Cerca de 50% do genoma dos vírus de DNA evoluiu direcionado para a manipulação de importantes funções celulares do hospedeiro. Estas estratégias são muito diversas e conferem ao vírus vantagens importantes sobre o sistema imunitário do hospedeiro. Esses genes são, por isso, potenciais fontes de informação para a geração de novos fármacos dirigidos à manipulação da resposta imunológica na saúde e na doença. Esta tese centra-se na análise da função de dois genes virais distintos, ambos com funções imunomoduladoras. O gene do Vírus da Peste Suína Africana codificado pela “open reading frame” I329L (ORF I329L), e o gene do vírus herpes-gama-68 de murino codificado pela “open reading frame” M2 (ORF M2). Ambos os vírus são conhecidos por codificar várias proteínas capazes de manipular componentes vitais da resposta antiviral. Neste trabalho nós demonstramos que tanto a ORF I329L quanto ORF M2 são capazes de manipular a imunidade inata ou adquirida.(...)
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Horridge, Jackie J. "RNA-protein interactions of the adenovirus proteins E1B 55K and E4 Orf6." Thesis, University of Warwick, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322435.

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Lindström, Hannah Kim. "Molecular studies of the hepatitis C virus : the role of IRES activity for therapy response, and the impact of the non-structural protein NS4B on the viral proliferation /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-875-4/.

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Weinmaster, Geraldine Ann. "Structural and functional characterization of the Fujinami sarcoma virus transforming protein." Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25991.

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The phosphorylation of the Fujinami sarcoma virus transforming protein (FSV P140gag-fps) is complex, reversible and affects its tyrosine specific protein kinase activity and transforming function. The sites of phosphorylation within FSV P140gag-fps have been localized to various regions of the protein using partial proteolysis. The two major phosphotyrosine residues and a major phosphoserine residue are located in the C-terminal portion of the fps region, which contains the kinase active domain. A comparative tryptic phosphopeptide analysis of the gag-fps proteins of three FSV variants shows that the phosphotyrosine containing peptides have similar mobilities. To determine whether tyrosine phosphorylation affects protein function and to evaluate the substrate specificity of the protein kinase intrinsic to FSV P130gag-fps oligonucleotide-directed mutagenesis was used to change tyrosine-1073, the major site of P130gag-fps phosphorylation. Tyrosine-1073 was mutated to a phenylalanine and a glycine, amino acids that cannot be phosphorylated, and to the other commonly phosphorylated hydroxyamino acids, serine and threonine. Neither serine nor threonine were phosphorylated when substituted for tyrosine-1073 indicating a strict specificity for and oncogenic capacities. These data indicate that tyrosine phosphorylation stimulates the biochemical and biological activities of FSV P130gag-fps and suggest that tyrosine phosphorylation modulates protein function. Mutations within the putative ATP-binding site of P130gag-fps at lysine-950 destroy both its kinase and transforming activities, supporting the idea that the tyrosine kinase activity intrinsic to P130gag-fps is essential for its transforming function. The mutant protein was also shown to be phosphorylated at a second tyrosine site, which has been previously identified in wild-type P130gag-fps as a site exclusively phosphorylated in vivo. Phosphorylation of secondary tyrosine residues within a mutant protein devoid of intrinsic tyrosine protein kinase activity suggests that the FSV P130gag-fps may be a target for phosphorylation by cellular tyrosine specific protein kinases.
Science, Faculty of
Microbiology and Immunology, Department of
Graduate
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Helt, Anna-Marija. "Multiple biological activities of the human papillomavirus type 16 E7 oncoprotein contribute to the abrogation of human epithelial cell cycle control /." Thesis, Connect to this title online; UW restricted, 2002. http://hdl.handle.net/1773/11514.

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Kim, Irene. "Mechanisms of Membrane Disruption by Viral Entry Proteins." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10192.

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To enter and infect cells, viruses must overcome the barrier presented by the cell membrane. Enveloped viruses, which possess their own lipid bilayer, fuse their viral membrane with the cell membrane. Non-enveloped viruses, whose outer surface is composed of proteins, penetrate through the hydrophobic interior of the cell membrane. Viruses accomplish the processes by coupling conformational changes in viral "entry proteins" to membrane disruption. This dissertation investigates the membrane disruption mechanisms of rotavirus, a non-enveloped virus, and vesicular stomatitis virus (VSV), an enveloped virus. Rotavirus uses proteins of its outer capsid to penetrate the membrane and deliver a transcriptionally-active core particle into the cell cytoplasm. \(VP5^*\), an outer capsid protein, undergoes a foldback rearrangement that translocates three clustered hydrophobic loops by \(\sim 180^{\circ}\). This rearrangement resembles the foldback rearrangements of enveloped virus fusion proteins. In the first half of my dissertation, I show that the hydrophobicity of the \(VP5^*\) apex is required for membrane disruption during rotavirus cell entry by mutating hydrophobic residues within the loop to hydrophilic residues. One particular mutation diminishes liposome interaction by the protein, blocks membrane penetration by virus particles in cells, and reduces particle infectivity by 10,000-fold. VSV uses its fusion protein, G, to fuse at low pH. Unlike other viral fusion proteins, pH-induced conformational changes in G are reversible. In the second half of my dissertation, I measure the fusion kinetics of individual VSV particles using a single-particle fusion assay previously developed for influenza virus. I find that hemifusion by VSV consists of at least two steps, an initial step that is pH-dependent and reversible, and a second step that is pH-independent. At low pHs, the second step becomes the sole rate-limiting step. I also show that at pH 6.6, the VSV particle enters a stable intermediate state that binds tightly to membranes but does not precede to fusion. This dissertation uses a variety of experimental approaches to arrive at a more detailed understanding of how viruses use their entry proteins to either penetrate or fuse with the cell membrane.
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Biggs, Thelma Elizabeth. "The effects of viral proteins on macrophage function." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285659.

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Casey, John P. Jr. "Capsid catalysis : de novo enzymes on viral proteins." Thesis, Massachusetts Institute of Technology, 2015. http://hdl.handle.net/1721.1/99052.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biological Engineering, 2015.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 107-119).
Biocatalysis has grown rapidly in recent decades as a solution to the evolving demands of industrial chemical processes. Mounting environmental pressures and shifting supply chains underscore the need for novel chemical activities, while rapid biotechnological progress has greatly increased the utility of enzymatic methods. Enzymes, though capable of high catalytic efficiency and remarkable reaction selectivity, still suffer from relative instability, high costs of scaling, and functional inflexibility. Herein, M13 bacteriophage libraries are engineered as a biochemical platform for de novo semisynthetic enzymes, functionally modular and widely stable. Carbonic anhydrase-inspired hydrolytic activity via Zn²+ coördination is first demonstrated. The phage clone identified hydrolyzes a range of carboxylic esters, is active from 25°C to 80°C, and displays greater catalytic efficacy in DMSO than in water. Reduction-oxidation activity is subsequently developed via heme and copper cofactors. Heme-phage complexes oxidize multiple peroxidase substrates in a pH-dependent manner. The same phage clone also binds copper(II) and oxidizes a catechol derivative, di-tert-butylcatechol, using atmospheric oxygen as a terminal oxidant. This clone could be purified from control phage via Cu-NTA columns, enabling future library selections for phage that coördinate Cu²+ ions. The M13 semisynthetic enzyme platform complements biocatalysts with characteristics of heterogeneous catalysis, yielding high-surface area, thermostable biochemical structures readily adaptable to reactions in myriad solvents. As the viral structure ensures semisynthetic enzymes remain linked to the genetic sequences responsible for catalysis, future work could tailor the biocatalysts to high-demand synthetic processes by evolving new activities, utilizing high-throughput screening technology and harnessing M13's multifunctionality.
by John P. Casey, Jr.
Ph. D.
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Eid, Fatma Elzahraa Sobhy. "Predicting the Interactions of Viral and Human Proteins." Diss., Virginia Tech, 2017. http://hdl.handle.net/10919/77581.

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The world has proven unprepared for deadly viral outbreaks. Designing antiviral drugs and strategies requires a firm understanding of the interactions taken place between the proteins of the virus and human proteins. The current computational models for predicting these interactions consider only single viruses for which extensive prior knowledge is available. The two prediction frameworks in this dissertation, DeNovo and DeNovo-Human, make it possible for the first time to predict the interactions between any viral protein and human proteins. They further helped to answer critical questions about the Zika virus. DeNovo utilizes concepts from virology, bioinformatics, and machine learning to make predictions for novel viruses possible. It pools protein-protein interactions (PPIs) from different viruses sharing the same host. It further introduces taxonomic partitioning to make the reported performance reflect the situation of predicting for a novel virus. DeNovo avoids the expected low accuracy of such a prediction by introducing a negative sampling scheme that is based on sequence similarity. DeNovo achieved accuracy up to 81% and 86% when predicting for a new viral species and a new viral family, respectively. This result is comparable to the best achieved previously in single virus-host and intra-species PPI prediction cases. DeNovo predicts PPIs of a novel virus without requiring known PPIs for it, but with a limitation on the number of human proteins it can make predictions against. The second framework, DeNovo-Human, relaxes this limitation by forcing in-network prediction and random sampling while keeping the pooling technique of DeNovo. The accuracy and AUC are both promising ($>85%$, and $>91%$ respectively). DeNovo-Human facilitates predicting the virus-human PPI network. To demonstrate how the two frameworks can enrich our knowledge about virus behavior, I use them to answer interesting questions about the Zika virus. The research questions examine how the Zika virus enters human cells, fights the innate immune system, and causes microcephaly. The answers obtained are well supported by recently published Zika virus studies.
Ph. D.
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Hahn, Young Shin Lim Strauss James H. Strauss James H. "Functional analysis of viral nonstructural and structural proteins /." Diss., Pasadena, Calif. : California Institute of Technology, 1989. http://resolver.caltech.edu/CaltechETD:etd-06072007-075259.

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Books on the topic "Viral proteins"

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Koszinowski, Ulrich H., and Hartmut Hengel, eds. Viral Proteins Counteracting Host Defenses. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-59421-2.

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H, Koszinowski U., and Hengel H, eds. Viral proteins counteracting host defenses. Berlin: Springer, 2002.

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W, Hicks Barry, ed. Viral applications of green fluorescent protein: Methods and protocols. Totowa, N.J: Humana, 2009.

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Dobert, Raymond. Viral resistance in plants, viral coat proteins: January 1991 - July 1996. Beltsville, Md: USDA, ARS, National Agricultural Library, 1996.

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Uversky, Vladimir N. Flexible viruses: Structural disorder in viral proteins. Hoboken: Wiley, 2012.

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Fischer, Wolfgang B., ed. Viral Membrane Proteins: Structure, Function, and Drug Design. Boston, MA: Springer US, 2005. http://dx.doi.org/10.1007/0-387-28146-0.

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Bridgen, Anne. Reverse genetics of RNA viruses: Applications and perspectives. Chichester, West Sussex: John Wiley & Sons, 2012.

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Joe, Bentz, ed. Viral fusion mechanisms. Boca Raton, Fla: CRC Press, 1993.

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International Symposium on the Immunobiology of Proteins and Peptides (3rd 1984 Tahoe City, Calif.). Immunobiology of proteins and peptides III: Viral and bacterial antigens. New York: Plenum Press, 1985.

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Sherwood, Casjens, ed. Virus structure and assembly. Boston: Jones and Bartlett, 1985.

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Book chapters on the topic "Viral proteins"

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Karyampudi, Lavakumar, and Keith L. Knutson. "Viral-Like Proteins." In Cancer Therapeutic Targets, 545–59. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4419-0717-2_147.

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Karyampudi, Lavakumar, and Keith L. Knutson. "Viral-Like Proteins." In Cancer Therapeutic Targets, 1–15. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6613-0_147-1.

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Shaw, A. L., R. Rothnagel, C. Q. Y. Zeng, J. A. Lawton, R. F. Ramig, M. K. Estes, and B. V. Venkataram Prasad. "Rotavirus structure: interactions between the structural proteins." In Viral Gastroenteritis, 21–27. Vienna: Springer Vienna, 1996. http://dx.doi.org/10.1007/978-3-7091-6553-9_3.

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Hildenbrand, Zacariah L., and Ricardo A. Bernal. "Chaperonin-Mediated Folding of Viral Proteins." In Viral Molecular Machines, 307–24. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0980-9_13.

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Modis, Yorgo. "Class II Fusion Proteins." In Viral Entry into Host Cells, 150–66. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7651-1_8.

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Sinkovics, Joseph G. "Viral and Cellular Proteins Interact." In RNA/DNA and Cancer, 247–50. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-22279-0_16.

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Dimmock, Nigel J. "Viral Carbohydrates, Proteins and Neutralization." In Current Topics in Microbiology and Immunology, 39–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-642-77849-0_12.

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Gerlich, W. H., K. H. Heermann, and Lu Xuanyong. "Functions of hepatitis B surface proteins." In Chronically Evolving Viral Hepatitis, 129–32. Vienna: Springer Vienna, 1992. http://dx.doi.org/10.1007/978-3-7091-5633-9_28.

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Oglesbee, Michael, Mi Young Kim, Yaoling Shu, and Sonia Longhi. "Extracellular HSP70, Neuroinflammation and Protection Against Viral Virulence." In Heat Shock Proteins, 23–55. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-02254-9_2.

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Soleimanjahi, Hoorieh, and Asghar Abdoli. "Role of Chaperone Mediated Autophagy in Viral Infections." In Heat Shock Proteins, 147–54. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-02254-9_7.

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Conference papers on the topic "Viral proteins"

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Schelbert, S., V. Dries, U. Drebber, M. Schindeldecker, A. Weinmann, R. Bartenschlager, P. Schirmacher, W. Roth, and BK Straub. "Lipid droplets and associated proteins in viral hepatitis." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677286.

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Smirnova, N., S. M. Yeligar, M. Ahmed, X. Fan, D. M. Guidot, and B. S. Staitieh. "HIV-Related Viral Proteins Impair Mitochondrial Function in Rat Alveolar Macrophages." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a5189.

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Graham, Daniel, and Yunjoo Bae. "Ternary Phase Diagrams of Viral Proteins: The Example of H1N1 Influenza." In MOL2NET 2018, International Conference on Multidisciplinary Sciences, 4th edition. Basel, Switzerland: MDPI, 2018. http://dx.doi.org/10.3390/mol2net-04-05900.

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Tu, T., B. Zehnder, M. Levy, G. Micali, L. Tran, O. Dabere, N. Main, N. Shackel, and S. Urban. "Hepatitis B virus (HBV) DNA integration is not driven by viral proteins." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677293.

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Gillock, Eric, Scott Rottinghaus, Avelina Paulsen, Scott Smiley, Deching Chang, Richard Consigli, and Deching Chang. "The effect of microgravity on the stability and assembly of viral proteins." In AIP Conference Proceedings Volume 387. ASCE, 1997. http://dx.doi.org/10.1063/1.52099.

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Sharma, G., M. Badescu, A. Dubey, C. Mavroidis, T. Sessa, S. M. Tomassone, and M. L. Yarmush. "Kinematics and Workspace Analysis of Protein Based Nano-Motors." In ASME 2004 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2004. http://dx.doi.org/10.1115/detc2004-57569.

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Kinematic and workspace analyses are performed to predict the performance of a new nanoscale biomolecular motor: The Viral Protein Linear (VPL) Motor. The motor is based on a conformational change observed in a family of viral envelope proteins when subjected to a changing pH environment. The conformational change produces a motion of about 10 nm, making the VPL a basic linear actuator, which can be further interfaced with other organic/inorganic nanoscale components such as DNA actuators and carbon nanotubes. This paper presents the principle of operation of the VPL motor and the development of direct and inverse kinematic models for workspace analysis. Preliminary results obtained from the developed computational tools are presented.
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Graham, Daniel, Samuel Barlow, Diego Cuculon, and Jordan Hauck. "Information Signatures of Viral Proteins: A Study of Influenza A Hemagglutinin and Neuraminidase." In MOL2NET, International Conference on Multidisciplinary Sciences. Basel, Switzerland: MDPI, 2015. http://dx.doi.org/10.3390/mol2net-1-b009.

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Nazarenko, E. A., and E. S. Starodubova. "CELL-SYNTHESIZED NON-STRUCTURAL PROTEIN 1 OF TICK-BORNE ENCEPHALITIS VIRUS IS ASSOCIATED WITH EXOSOMES AND INCREASE THEIR SECRETION." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-257.

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Recent studies propose the importance of extracellular vesicles (EVs) in the pathogenesis of tick-borne encephalitis virus (TBEV), but the involvement of individual viral proteins on them has not yet been studied. In this work, it was shown that the expression of TBEV nonstructural protein 1 (NS1) in cells increases the secretion of EVs. It has been established that NS1 is found in the fraction of exosomes obtained by precipitation, as well as by chromatography of cell culture media.
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Jessup, J. Milburn, Abid R. Mattoo, and Nikolay Korokhov. "Abstract 4216: Targeting NANOG: genes, proteins and response to viral RNAi in preclinical models." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-4216.

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"Expression of sheep pox viral A27L and L1R proteins in prokaryotic and eukaryotic systems." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, 2019. http://dx.doi.org/10.18699/plantgen2019-023.

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Reports on the topic "Viral proteins"

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Gafni, Yedidya, and Vitaly Citovsky. Molecular interactions of TYLCV capsid protein during assembly of viral particles. United States Department of Agriculture, April 2007. http://dx.doi.org/10.32747/2007.7587233.bard.

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Tomato yellow leaf curl geminivirus (TYLCV) is a major pathogen of cultivated tomato, causing up to 100% crop loss in many parts of the world. The present proposal, a continuation of a BARD-funded project, expanded our understanding of the molecular mechanisms by which CP molecules, as well as its pre-coat partner V2, interact with each other (CP), with the viral genome, and with cellular proteins during assembly and movement of the infectious virions. Specifically, two major objectives were proposed: I. To study in detail the molecular interactions between CP molecules and between CP and ssDNA leading to assembly of infectious TYLCV virions. II. To study the roles of host cell factors in TYLCV assembly. Our research toward these goals has produced the following major achievements: • Characterization of the CP nuclear shuttling interactor, karyopherin alpha 1, its pattern of expression and the putative involvement of auxin in regulation of its expression. (#1 in our list of publication, Mizrachy, Dabush et al. 2004). • Identify a single amino acid in the capsid protein’s sequence that is critical for normal virus life-cycle. (#2 in our list of publications, Yaakov, Levy et al. in preparation). • Development of monoclonal antibodies with high specificity to the capsid protein of TYLCV. (#3 in our list of publications, Solmensky, Zrachya et al. in press). • Generation of Tomato plants resistant to TYLCV by expressing transgene coding for siRNA targeted at the TYLCV CP. (#4 in our list of publications, Zrachya, Kumar et al. in press). •These research findings provided significant insights into (i) the molecular interactions of TYLCV capsid protein with the host cell nuclear shuttling receptor, and (ii) the mechanism by which TYLCV V2 is involved in the silencing of PTGS and contributes to the virus pathogenicity effect. Furthermore, the obtained knowledge helped us to develop specific strategies to attenuate TYLCV infection, for example, by blocking viral entry into and/or exit out of the host cell nucleus via siRNA as we showed in our publication recently (# 4 in our list of publications). Finally, in addition to the study of TYLCV nuclear import and export, our research contributed to our understanding of general mechanisms for nucleocytoplasmic shuttling of proteins and nucleic acids in plant cells. Also integration for stable transformation of ssDNA mediated by our model pathogen Agrobacterium tumefaciens led to identification of plant specific proteins involved.
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Lapidot, Moshe, and Vitaly Citovsky. molecular mechanism for the Tomato yellow leaf curl virus resistance at the ty-5 locus. United States Department of Agriculture, January 2016. http://dx.doi.org/10.32747/2016.7604274.bard.

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Tomato yellow leaf curl virus (TYLCV) is a major pathogen of tomato that causes extensive crop loss worldwide, including the US and Israel. Genetic resistance in the host plant is considered highly effective in the defense against viral infection in the field. Thus, the best way to reduce yield losses due to TYLCV is by breeding tomatoes resistant or tolerant to the virus. To date, only six major TYLCV-resistance loci, termed Ty-1 to Ty-6, have been characterized and mapped to the tomato genome. Among tomato TYLCV-resistant lines containing these loci, we have identified a major recessive quantitative trait locus (QTL) that was mapped to chromosome 4 and designated ty-5. Recently, we identified the gene responsible for the TYLCV resistance at the ty-5 locus as the tomato homolog of the gene encoding messenger RNA surveillance factor Pelota (Pelo). A single amino acid change in the protein is responsible for the resistant phenotype. Pelo is known to participate in the ribosome-recycling phase of protein biosynthesis. Our hypothesis was that the resistant allele of Pelo is a “loss-of-function” mutant, and inhibits or slows-down ribosome recycling. This will negatively affect viral (as well as host-plant) protein synthesis, which may result in slower infection progression. Hence we have proposed the following research objectives: Aim 1: The effect of Pelota on translation of TYLCV proteins: The goal of this objective is to test the effect Pelota may or may not have upon translation of TYLCV proteins following infection of a resistant host. Aim 2: Identify and characterize Pelota cellular localization and interaction with TYLCV proteins: The goal of this objective is to characterize the cellular localization of both Pelota alleles, the TYLCV-resistant and the susceptible allele, to see whether this localization changes following TYLCV infection, and to find out which TYLCV protein interacts with Pelota. Our results demonstrate that upon TYLCV-infection the resistant allele of pelota has a negative effect on viral replication and RNA transcription. It is also shown that pelota interacts with the viral C1 protein, which is the only viral protein essential for TYLCV replication. Following subcellular localization of C1 and Pelota it was found that both protein localize to the same subcellular compartments. This research is innovative and potentially transformative because the role of Peloin plant virus resistance is novel, and understanding its mechanism will lay the foundation for designing new antiviral protection strategies that target translation of viral proteins. BARD Report - Project 4953 Page 2
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Grubman, Marvin J., Yehuda Stram, Peter W. Mason, and Hagai Yadin. Development of an Empty Viral Capsid Vaccine against Foot and Mouth Disease. United States Department of Agriculture, August 1995. http://dx.doi.org/10.32747/1995.7570568.bard.

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Foot-and-mouth disease (FMD), a highly infectious viral disease of cloven-hoofed animals, is economically the most important disease of domestic animals. Although inactivated FMD vaccines have been succesfully used as part of comprehensive eradication programs in Western Europe, there are a number of concerns about their safety. In this proposal, we have attempted to develop a new generation of FMD vaccines that addresses these concerns. Specifically we have cloned the region of the viral genome coding for the structural proteins and the proteinase responsible for processing of the structural protein precursor into both a DNA vector and a replication-deficient human adenovirus. We have demonstrated the induction of an FMDV-specific immune response and a neutralizing antibody response with the DNA vectors in mice, but preliminary potency and efficacy studies in swine are variable. However, the adenovirus vector induces a significant and long-lived neutralizing antibody response in mice and most importantly a neutralizing and protective response in swine. These results suggest that the empty capsid approach is a potential alternative to the current vaccination strategy.
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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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Citovsky, Vitaly, and Yedidya Gafni. Suppression of RNA Silencing by TYLCV During Viral Infection. United States Department of Agriculture, December 2009. http://dx.doi.org/10.32747/2009.7592126.bard.

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The Israeli isolate of Tomato yellow leaf curl geminivirus (TYLCV-Is) is a major tomato pathogen, causing extensive (up to 100%) crop losses in Israel and in the south-eastern U.S. (e.g., Georgia, Florida). Surprisingly, however, little is known about the molecular mechanisms of TYLCV-Is interactions with tomato cells. In the current BARD project, we have identified a TYLCV-Is protein, V2, which acts as a suppressor of RNA silencing, and showed that V2 interacts with the tomato (L. esculentum) member of the SGS3 (LeSGS3) protein family known to be involved in RNA silencing. This proposal will use our data as a foundation to study one of the most intriguing, yet poorly understood, aspects of TYLCV-Is interactions with its host plants – possible involvement of the host innate immune system, i.e., RNA silencing, in plant defense against TYLCV-Is and the molecular pathway(s) by which TYLCV-Is may counter this defense. Our project sought two objectives: I. Study of the roles of RNA silencing and its suppression by V2 in TYLCV-Is infection of tomato plants. II. Study of the mechanism by which V2 suppresses RNA silencing. Our research towards these goals has produced the following main achievements: • Identification and characterization of TYLCV V2 protein as a suppressor of RNA silencing. (#1 in the list of publications). • Characterization of the V2 protein as a cytoplasmic protein interacting with the plant protein SlSGS3 and localized mainly in specific, not yet identified, bodies. (#2 in the list of publications). • Development of new tools to study subcellular localization of interacting proteins (#3 in the list of publications). • Characterization of TYLCV V2 as a F-BOX protein and its possible role in target protein(s) degradation. • Characterization of TYLCV V2 interaction with a tomato cystein protease that acts as an anti-viral agent. These research findings provided significant insights into (I) the suppression of RNA silencing executed by the TYLCV V2 protein and (II) characterization some parts of the mechanism(s) involved in this suppression. The obtained knowledge will help to develop specific strategies to attenuate TYLCV infection, for example, by blocking the activity of the viral suppressor of gene silencing thus enabling the host cell silencing machinery combat the virus.
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Wang, X. F., and M. Schuldiner. Systems biology approaches to dissect virus-host interactions to develop crops with broad-spectrum virus resistance. Israel: United States-Israel Binational Agricultural Research and Development Fund, 2020. http://dx.doi.org/10.32747/2020.8134163.bard.

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More than 60% of plant viruses are positive-strand RNA viruses that cause billion-dollar losses annually and pose a major threat to stable agricultural production, including cucumber mosaic virus (CMV) that infects numerous vegetables and ornamental trees. A highly conserved feature among these viruses is that they form viral replication complexes (VRCs) to multiply their genomes by hijacking host proteins and remodeling host intracellular membranes. As a conserved and indispensable process, VRC assembly also represents an excellent target for the development of antiviral strategies that can be used to control a wide-range of viruses. Using CMV and a model virus, brome mosaic virus (BMV), and relying on genomic tools and tailor-made large-scale resources specific for the project, our original objectives were to: 1) Identify host proteins that are required for viral replication complex assembly. 2) Dissect host requirements that determine viral host range. 3) Provide proof-of-concept evidence of a viral control strategy by blocking the viral replication complex-localized phospholipid synthesis. We expect to provide new ways and new concepts to control multiple viruses by targeting a conserved feature among positive-strand RNA viruses based on our results. Our work is going according to the expected timeline and we are progressing well on all aims. For Objective 1, among ~6,000 yeast genes, we have identified 96 hits that were possibly play critical roles in viral replication. These hits are involved in cellular pathways of 1) Phospholipid synthesis; 2) Membrane-shaping; 3) Sterol synthesis and transport; 4) Protein transport; 5) Protein modification, among many others. We are pursuing several genes involved in lipid metabolism and transport because cellular membranes are primarily composed of lipids and lipid compositional changes affect VRC formation and functions. For Objective 2, we have found that CPR5 proteins from monocotyledon plants promoted BMV replication while those from dicotyledon plants inhibited it, providing direct evidence that CPR5 protein determines the host range of BMV. We are currently examining the mechanisms by which dicot CPR5 genes inhibit BMV replication and expressing the dicot CPR5 genes in monocot plants to control BMV infection. For Objective 3, we have demonstrated that substitutions in a host gene involved in lipid synthesis, CHO2, prevented the VRC formation by directing BMV replication protein 1a (BMV 1a), which remodels the nuclear membrane to form VRCs, away from the nuclear membrane, and thus, no VRCs were formed. This has been reported in Journal of Biological Chemistry. Based on the results from Objective 3, we have extended our plan to demonstrate that an amphipathic alpha-helix in BMV 1a is necessary and sufficient to target BMV 1a to the nuclear membrane. We further found that the counterparts of the BMV 1a helix from a group of viruses in the alphavirus-like superfamily, such as CMV, hepatitis E virus, and Rubella virus, are sufficient to target VRCs to the designated membranes, revealing a conserved feature among the superfamily. A joint manuscript describing these exciting results and authored by the two labs will be submitted shortly. We have also successfully set up systems in tomato plants: 1) to efficiently knock down gene expression via virus-induced gene silencing so we could test effects of lacking a host gene(s) on CMV replication; 2) to overexpress any gene transiently from a mild virus (potato virus X) so we could test effects of the overexpressed gene(s) on CMV replication. In summary, we have made promising progress in all three Objectives. We have identified multiple new host proteins that are involved in VRC formation and may serve as good targets to develop antiviral strategies; have confirmed that CPR5 from dicot plants inhibited viral infection and are generating BMV-resistance rice and wheat crops by overexpressing dicot CPR5 genes; have demonstrated to block viral replication by preventing viral replication protein from targeting to the designated organelle membranes for the VRC formation and this concept can be further employed for virus control. We are grateful to BARD funding and are excited to carry on this project in collaboration.
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Mawassi, Munir, and Valerian V. Dolja. Role of the viral AlkB homologs in RNA repair. United States Department of Agriculture, June 2014. http://dx.doi.org/10.32747/2014.7594396.bard.

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AlkB proteins that repair DNA via reversing methylation damage are conserved in a broad range of prokaryotes and eukaryotes including plants. Surprisingly, AlkB-domains were discovered in the genomes of numerous plant positive-strand RNA viruses, majority of which belong to the family Flexiviridae. The major goal of this research was to reveal the AlkB functions in the viral infection cycle using a range of complementary genetic and biochemical approaches. Our hypotheses was that AlkB is required for efficient replication and genetic stability of viral RNA genomes The major objectives of the research were to identify the functions of GVA AlkB domain throughout the virus infection cycle in N. benthamiana and grapevine, to investigate possible RNA silencing suppression activity of the viral AlkBs, and to characterize the RNA demethylation activity of the mutated GVA AlkBs in vitro and in vivo to determine methylation status of the viral RNA. Over the duration of project, we have made a very substantial progress with the first two objectives. Because of the extreme low titer of the virus particles in plants infected with the AlkB mutant viruses, we were unable to analyze RNA demethylation activity and therefore had to abandon third objective. The major achievements with our objectives were demonstration of the AlkB function in virus spread and accumulation in both experimental and natural hosts of GVA, discovery of the functional cooperation and physical interaction between AlkB and p10 AlkB in suppression of plant RNA silencing response, developing a powerful virus vector technology for grapevine using GLRaV-2-derived vectors for functional genomics and pathogen control in grapevine, and in addition we used massive parallel sequencing of siRNAs to conduct comparative analysis of the siRNA populations in grape plants infected with AlkB-containing GLRaV-3 versus GLRaV-2 that does not encode AlkB. This analysis revealed dramatically reduced levels of virus-specific siRNAs in plants infected with GLRaV-3 compared to that in GLRaV-2 infection implicating AlkB in suppression of siRNA formation. We are pleased to report that BARD funding resulted in 5 publications directly supported by BARD, one US patent, and 9 more publications also relevant to project. Moreover, two joint manuscripts that summarize work on GVA AlkB (led by Israeli PI) and on viral siRNAs in grapevine (led by US PI in collaboration with University of Basel) are in preparation.
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Wolf, Shmuel, and William J. Lucas. Involvement of the TMV-MP in the Control of Carbon Metabolism and Partitioning in Transgenic Plants. United States Department of Agriculture, October 1999. http://dx.doi.org/10.32747/1999.7570560.bard.

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The function of the 30-kilodalton movement protein (MP) of tobacco mosaic virus (TMV) is to facilitate cell-to-cell movement of viral progeny in infected plants. Our earlier findings have indicated that this protein has a direct effect on plasmodesmal function. In addition, these studies demonstrated that constitutive expression of the TMV MP gene (under the control of the CaMV 35S promoter) in transgenic tobacco plants significantly affects carbon metabolism in source leaves and alters the biomass distribution between the various plant organs. The long-term goal of the proposed research was to better understand the factors controlling carbon translocation in plants. The specific objectives were: A) To introduce into tobacco and potato plants a virally-encoded (TMV-MP) gene that affects plasmodesmal functioning and photosynthate partitioning under tissue-specific promoters. B) To introduce into tobacco and potato plants the TMV-MP gene under the control of promoters which are tightly repressed by the Tn10-encoded Tet repressor, to enable the expression of the protein by external application of tetracycline. C) To explore the mechanism by which the TMV-MP interacts with the endogenous control o~ carbon allocation. Data obtained in our previous project together with the results of this current study established that the TMV-MP has pleiotropic effects when expressed in transgenic tobacco plants. In addition to its ability to increase the plasmodesmal size exclusion limit, it alters carbohydrate metabolism in source leaves and dry matter partitioning between the various plant organs, Expression of the TMV-MP in various tissues of transgenic potato plants indicated that sugars and starch levels in source leaves are reduced below those of control plants when the TMV-MP is expressed in green tissue only. However, when the TMV-MP was expressed predominantly in PP and CC, sugar and starch levels were raised above those of control plants. Perhaps the most significant result obtained from experiments performed on transgenic potato plants was the discovery that the influence of the TMV-MP on carbohydrate allocation within source leaves was under developmental control and was exerted only during tuber development. The complexity of the mode by which the TMV-MP exerts its effect on the process of carbohydrate allocation was further demonstrated when transgenic tobacco plants were subjected to environmental stresses such as drought stress and nutrients deficiencies, Collectively, these studies indicated that the influence of the TMV-MP on carbon allocation L the result of protein-protein interaction within the source tissue. Based on these results, together with the findings that plasmodesmata potentiate the cell-to-cell trafficking of viral and endogenous proteins and nucleoproteins complexes, we developed the theme that at the whole plant level, the phloem serves as an information superhighway. Such a long-distance communication system may utilize a new class of signaling molecules (proteins and/or RNA) to co-ordinate photosynthesis and carbon/nitrogen metabolism in source leaves with the complex growth requirements of the plant under the prevailing environmental conditions. The discovery that expression of viral MP in plants can induce precise changes in carbon metabolism and photoassimilate allocation, now provide a conceptual foundation for future studies aimed at elucidating the communication network responsible for integrating photosynthetic productivity with resource allocation at the whole-plant level. Such information will surely provide an understanding of how plants coordinate the essential physiological functions performed by distantly-separated organs. Identification of the proteins involved in mediating and controlling cell-to-cell transport, especially at the companion cell-sieve element boundary, will provide an important first step towards achieving this goal.
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Citovsky, Vitaly, and Yedidya Gafni. Viral and Host Cell Determinants of Nuclear Import and Export of the Tomato Yellow Leaf Curl Virus in Tomato Plants. United States Department of Agriculture, August 2002. http://dx.doi.org/10.32747/2002.7585200.bard.

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Tomato yellow leaf curl geminivirus (TYLCV) is a major pathogen of cultivated tomato, causing up to 100% crop loss in many parts of the world. In Israel, where TYLCV epidemics have been recorded since the 1960' s, this viral disease is well known and has been of economic significance ever since. In recent years, TYLCV outbreaks also occurred in the "New World" - Cuba, The Dominican Republic, and in the USA, in Florida, Georgia and Louisiana. Thus, TYLCV substantially hinders tomato growth throughout the world. Surprisingly, however, little is known about the molecular mechanisms of TYLCV interaction with the host tomato cells. The present proposal, a continuation of the project supported by BARD from 1994, expanded our understanding of the molecular mechanisms by which TYLCV enters the host cell nucleus for replication and transcription and exits it for the subsequent cell-to-cell spread. Our project sought two objectives: I. To study the roles of the viral capsid protein (CP) and host cell factors in TYLCV nuclear import. II. To study the roles of CP and host cell factors in TYLCV nuclear export. Our research toward these goals have produced the following major achievements: . Developed a one-hybrid assay for protein nuclear export and import (#3 in the List of Publications). . Identified a functional nuclear export signal (NES) in the capsid protein (CP) of TYLCV (#3 in the List of Publications). . Discovered homotypic interactions between intact TYLCV CP molecules and analyzed these interactions using deletion mutagenesis of TYLCV CP (#5 in the List of Publications). . Showed developmental and tissue-specific expression of the host factor required for nuclear import of TYLCV CP, tomato karyopherin alpha 1, in transgenic tomato plants (#14 in the List of Publications). . By analogy to nuclear import of TYLCV ,identified an Arabidopsis VIPI protein that participates in nuclear import of Agrobacterium T -complexes via the karyopherin alpha pathway (#4,6, and 8 in the List of Publications). These research findings provided significant insights into (i) the molecular pathway of TYLCV entry into the host cell nucleus, and (ii) the mechanism by which TYLCV is exported from the nucleus for the cell-to-cell spread of infection. Furthermore, the obtained knowledge will help to develop specific strategies to attenuate TYLCV infection, for example, by blocking viral entry into and/or exit out of the host cell nucleus. Also, as much of our findings is relevant to all geminiviruses, new anti- TYLCV approaches developed based on the results of our research will be useful to combat other members of the Geminivirus family. Finally, in addition to the study of TYLCV nuclear import and export, our research contributed to our understanding of general mechanisms for nucleocytoplasmic shuttling of proteins and nucleic acids in plant cells.
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Ehrlich, Marcelo, John S. Parker, and Terence S. Dermody. Development of a Plasmid-Based Reverse Genetics System for the Bluetongue and Epizootic Hemorrhagic Disease Viruses to Allow a Comparative Characterization of the Function of the NS3 Viroporin in Viral Egress. United States Department of Agriculture, September 2013. http://dx.doi.org/10.32747/2013.7699840.bard.

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Project Title: "Development of a plasmid-based reverse genetics system for the Bluetongue and Epizootic Hemorrhagic Disease viruses to allow comparative characterization of the function of the NS3 viroporin in viral egress". Project details: No - IS-4192-09; Participants – Ehrlich M. (Tel Aviv University), Parker J.S. (Cornell University), DermodyT.S. (Vanderbilt University); Period - 2009-2013. Orbiviruses are insect-borne infectious agents of ruminants that cause diseases with considerable economical impact in Israel and the United States. The recent outbreaks of BTV in Europe and of Epizootic Hemorrhagic Disease Virus (EHDV) in Israel, underscore the need for: (i) a better comprehension of the infection process of orbiviruses, (ii) the identification of unique vs. common traits among different orbiviruses, (iii) the development of novel diagnosis and treatment techniques and approaches; all aimed at the achievement of more effective control and treatment measures. It is the context of these broad goals that the present project was carried out. To fulfill our long-term goal of identifying specific viral determinants of virulence, growth, and transmission of the orbiviruses, we proposed to: (i) develop reverse genetics systems for BTV and EHDV2-Ibaraki; and (ii) identify the molecular determinants of the NS3 nonstructural protein related to viroporin/viral egress activities. The first objective was pursued with a two-pronged approach: (i) development of a plasmid-based reverse genetics system for BTV-17, and (ii) development of an "in-vitro" transcription-based reverse genetics system for EHDV2-Ibaraki. Both approaches encountered technical problems that hampered their achievement. However, dissection of the possible causes of the failure to achieve viral spread of EHDV2-Ibaraki, following the transfection of in-vitro transcribed genomic segments of the virus, revealed a novel characteristic of EHDV2-Ibaraki infection: an uncharacteristically low fold increase in titer upon infection of different cell models. To address the function and regulation of NS3 we employed the following approaches: (i) development (together with Anima Cell Metrology) of a novel technique (based on the transfection of fluorescently-labeledtRNAs) that allows for the detection of the levels of synthesis of individual viral proteins (i.e. NS3) in single cells; (ii) development of a siRNA-mediated knockdown approach for the reduction in levels of expression of NS3 in EHDV2-Ibaraki infected cells; (iii) biochemical and microscopy-based analysis of the localization, levels and post-translational modifications of NS3 in infected cells. In addition, we identified the altered regulation and spatial compartmentalization of protein synthesis in cells infected with EHDV2-Ibaraki or the mammalian reovirus. In EHDV2-Ibaraki-infected cells such altered regulation in protein synthesis occurs in the context of a cell stress reponse that includes the induction of apoptosis, autophagy and activation of the stressrelated kinase c-Jun N-terminal Kinase (JNK). Interestingly, inhibition of such stress-related cellular processes diminishes the production of infectious virions, suggesting that EHDV usurps these responses for the benefit of efficient infection. Taken together, while the present project fell short of the generation of novel reverse genetics systems for orbiviruses, the development of novel experimental approaches and techniques, and their employment in the analysis of EHDV-infected cells, yielded novel insights in the interactions of orbiviruses with mammalian cells.
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