Relevant bibliographies by topics / Virus interactions

Academic literature on the topic 'Virus interactions'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Virus interactions.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Virus interactions"

1

Strebel, Klaus. "Virus–host interactions." AIDS 17, Supplement 4 (2003): S25—S34. http://dx.doi.org/10.1097/00002030-200317004-00003.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Stebbing, Justin, and Brian Gazzard. "Virus host interactions." Obstetrician & Gynaecologist 5, no. 2 (April 2003): 103–6. http://dx.doi.org/10.1576/toag.5.2.103.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Calderwood, Michael A., Kavitha Venkatesan, Li Xing, Michael R. Chase, Alexei Vazquez, Amy M. Holthaus, Alexandra E. Ewence, et al. "Epstein–Barr virus and virus human protein interaction maps." Proceedings of the National Academy of Sciences 104, no. 18 (April 19, 2007): 7606–11. http://dx.doi.org/10.1073/pnas.0702332104.

Full text
Abstract:
A comprehensive mapping of interactions among Epstein–Barr virus (EBV) proteins and interactions of EBV proteins with human proteins should provide specific hypotheses and a broad perspective on EBV strategies for replication and persistence. Interactions of EBV proteins with each other and with human proteins were assessed by using a stringent high-throughput yeast two-hybrid system. Overall, 43 interactions between EBV proteins and 173 interactions between EBV and human proteins were identified. EBV–EBV and EBV–human protein interaction, or “interactome” maps provided a framework for hypotheses of protein function. For example, LF2, an EBV protein of unknown function interacted with the EBV immediate early R transactivator (Rta) and was found to inhibit Rta transactivation. From a broader perspective, EBV genes can be divided into two evolutionary classes, “core” genes, which are conserved across all herpesviruses and subfamily specific, or “noncore” genes. Our EBV–EBV interactome map is enriched for interactions among proteins in the same evolutionary class. Furthermore, human proteins targeted by EBV proteins were enriched for highly connected or “hub” proteins and for proteins with relatively short paths to all other proteins in the human interactome network. Targeting of hubs might be an efficient mechanism for EBV reorganization of cellular processes.
APA, Harvard, Vancouver, ISO, and other styles
4

Roy, Urmi. "Host–Virus Interactions in Japanese Encephalitis Virus." Zoonotic Diseases 2, no. 3 (August 5, 2022): 117–25. http://dx.doi.org/10.3390/zoonoticdis2030012.

Full text
Abstract:
Japanese encephalitis (JE) is a mosquito-borne zoonotic disease that causes severe brain inflammation. The JE virus envelope protein domain III (JEV-ED3) plays a critical role in activating receptor binding and membrane fusion. This communication briefly describes, in a computational approach, how structural changes within the JEV-ED3 mutant epitopes suppress their antibody neutralization function. The simulated results demonstrate that mutant Ser40Lys acts as an antibody neutralization escape while Asp41Arg may play the role of an escape mutant. Additionally, an examination of the double mutants on JEV-ED3 suggests that these mutants may qualify as stronger neutralizing escape agents than their single variants. The structural analysis of this work helps to identify the proper antiviral target sequences and specific monoclonal antibodies for the JEV-ED3 escape mutants.
APA, Harvard, Vancouver, ISO, and other styles
5

Pawlotsky, J. M. "Hepatitis C virus infection: virus/host interactions." Journal of Viral Hepatitis 5, s1 (September 1998): 3–8. http://dx.doi.org/10.1046/j.1365-2893.1998.0050s1003.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Segredo-Otero, Ernesto, and Rafael Sanjuán. "Cooperative Virus-Virus Interactions: An Evolutionary Perspective." BioDesign Research 2022 (October 3, 2022): 1–13. http://dx.doi.org/10.34133/2022/9819272.

Full text
Abstract:
Despite extensive evidence of virus-virus interactions, not much is known about their biological significance. Importantly, virus-virus interactions could have evolved as a form of cooperation or simply be a by-product of other processes. Here, we review and discuss different types of virus-virus interactions from the point of view of social evolution, which provides a well-established framework for interpreting the fitness costs and benefits of such traits. We also classify interactions according to their mechanisms of action and speculate on their evolutionary implications. As in any other biological system, the evolutionary stability of viral cooperation critically requires cheaters to be excluded from cooperative interactions. We discuss how cheater viruses exploit cooperative traits and how viral populations are able to counteract this maladaptive process.
APA, Harvard, Vancouver, ISO, and other styles
7

DaPalma, T., B. P. Doonan, N. M. Trager, and L. M. Kasman. "A systematic approach to virus–virus interactions." Virus Research 149, no. 1 (April 2010): 1–9. http://dx.doi.org/10.1016/j.virusres.2010.01.002.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Cook, Helen, Nadezhda Doncheva, Damian Szklarczyk, Christian von Mering, and Lars Jensen. "Viruses.STRING: A Virus-Host Protein-Protein Interaction Database." Viruses 10, no. 10 (September 23, 2018): 519. http://dx.doi.org/10.3390/v10100519.

Full text
Abstract:
As viruses continue to pose risks to global health, having a better understanding of virus–host protein–protein interactions aids in the development of treatments and vaccines. Here, we introduce Viruses.STRING, a protein–protein interaction database specifically catering to virus–virus and virus–host interactions. This database combines evidence from experimental and text-mining channels to provide combined probabilities for interactions between viral and host proteins. The database contains 177,425 interactions between 239 viruses and 319 hosts. The database is publicly available at viruses.string-db.org, and the interaction data can also be accessed through the latest version of the Cytoscape STRING app.
APA, Harvard, Vancouver, ISO, and other styles
9

Hoenen, Thomas, and Allison Groseth. "Virus–Host Cell Interactions." Cells 11, no. 5 (February 25, 2022): 804. http://dx.doi.org/10.3390/cells11050804.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Coffey, Lark, Anna-Bella Failloux, and Scott Weaver. "Chikungunya Virus–Vector Interactions." Viruses 6, no. 11 (November 24, 2014): 4628–63. http://dx.doi.org/10.3390/v6114628.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Virus interactions"

1

Murray, Shannon. "Foamy virus-host interactions /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/4987.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Quax, Tessa. "Archaeal virus-host interactions." Paris 6, 2013. http://www.theses.fr/2013PA066637.

Full text
Abstract:
The work presented in this thesis provides novel insights in several aspects of the molecular biology of Archaea, Bacteria and their viruses. The archaeal virus Sulfolobus islandicus rod-shaped virus 2 (SIRV2), has a remarkable infection cycle. Infection with SIRV2 results in the formation of large virus associated pyramids (VAPs) on the host cell surface. The pyramids open during the final step of the infection cycle, to allow the release of virions. This virus release mechanism is unique. The VAPs are formed by self-assembly of one virus-encoded protein, PVAP. VAPs exist as discrete particles, and are baseless pyramids with heptagonal perimeter. The assembly process of the VAPs is described, based on cryo-electron tomography experiments and mutational analysis of PVAP. VAPs consists of two layers of which the outer one continuous with the cell membrane. PVAP expression in bacterial and eukaryotic cells resulted in VAP formation on nearly all membranes, demonstrating that PVAP serves as a universal membrane remodeling system, which might be exploited for biotechnological purposes. Whole transcriptome sequencing allowed determination of a global map of virus and host gene expression during the infection cycle. Host genes involved in anti-viral defence are activated (i. E. CRISPR-Cas and toxin anti-toxin systems). The multi-subunit protein complexes crucial for CRISPR anti-viral defence have an uneven stoichiometry and are encoded on operons. It is shown that differential translation is a key determinant of modulated expression of genes clustered in operons and that codon bias generally is the best in silico indicator of unequal protein production
Le travail présenté dans cette thèse donne un nouveau regard sur plusieurs aspects de biologie moléculaire des archées, des bactéries et de leurs virus. Le virus Sulfolobus islandicus rod-shaped 2 (SIRV2) a un cycle d’infection remarquable. L’infection par SIRV2 aboutit à la formation sur la surface de la cellule hôte de grandes structures pyramidales associées à ce virus (VAP). Ce mécanisme de libération du virus SIRV2 est unique. Les VAPs sont formées par l’auto-assemblage de la protéine PVAP codée par le virus. Les VAPS peuvent être isolées sous forme de structures compactes et correspondent à des pyramides heptagonales creuses. Le processus d’assemblage des VAPs est décrit, d’après des expériences de cryo-tomographie et d’analyse mutationnelle de PVAP. Les VAPS sont constituées de deux couches dont celle extérieure continue avec la membrane cellulaire. L’expression des PVAP dans les cellules bactériennes et eucaryotiques conduit à la formation de VAPs sur presque toutes les membranes, ce qui démontre que PVAP sert comme un système universel de remodelage des membranes, qui pourrait être utilisé à des fins biotechnologiques. Le séquençage du transcriptome a permis la détermination d’une carte générale de l’expression génique du virus et de l’hôte pendant le cycle d’infection. Les gènes de l’hôte impliqués dans la défense anti-virale sont activés (systèmes CRISPR-Cas et toxine-antitoxine). Il a été démontré que la traduction différentielle est une clef déterminante de l’expression modulée des gènes groupés en opérons et que le biais de codon est généralement le meilleur indicateur in silico de production inégale de protéines
APA, Harvard, Vancouver, ISO, and other styles
3

Asare-Bediako, Elvis. "Brassicaceae : Turnip yellows virus interactions." Thesis, University of Warwick, 2011. http://wrap.warwick.ac.uk/44041/.

Full text
Abstract:
Turnip yellows virus (TuYV) is the most common and important virus infecting oilseed rape (Brassica napus) in the UK. It causes reductions in growth and seed yield in oilseed rape. Between 2007 and 2010, the prevalence of TuYV in oilseed rape crops in Lincolnshire, Warwickshire and Yorkshire was determined; incidences of infection ranged from 0 and 100%. The highest levels of infection were detected in Lincolnshire and the lowest in Yorkshire. Highest incidences were recorded during 2009-10 and the lowest in 2008-9. Incidences of TuYV were closely related to the flight activities Myzus persicae vector. Most fields showed slightly aggregated pattern of infection during autumn but spring sampling revealed more random patterns. Phylogenetic analysis of both nucleotide and amino acid sequences of the P0 and P3 genes of TuYY revealed three and two genetic groups of TuYV respectively, infecting oilseed rape in Lincolnshire, Warwickshire and Yorkshire. The P0 gene was more variable than the P3 gene and both were under purifying selection. TuYV populations in the three regions were highly structured with limited gene flow between them. Analysis of molecular variance (AMOVA) indicated 96- 97% of the observed variation was due to the variation between isolates within fields. Three RT-PCR assays were developed to differentiate the three genotypes. They successfully detected and discriminated isolates of the two major genotypes from oilseed rape in Lincolnshire. Twenty seven accessions of a B. napus Diversity Fixed Foundation Set (DFFS) screened for resistance against TuYV infections varied in their susceptibility to the virus. An accession Yudal had partial resistance to some but not all the isolates of the two major genetic groups tested. TuYV caused yield losses of up to 44.7% in a glasshouse experiment. A major QTL for the partial TuYV resistance was detected on chromosome C4 (N14), explaining up to 50.5% of the observed resistance.
APA, Harvard, Vancouver, ISO, and other styles
4

Ward, Rebecca. "Bluetongue virus non-structural protein 1 : virus-host interactions." Thesis, London School of Hygiene and Tropical Medicine (University of London), 2006. http://researchonline.lshtm.ac.uk/4646527/.

Full text
Abstract:
Bluetongue virus (BTY) is an orbivirus of the Reoviridae family that infects sheep and other ruminants. BTY has three non-structural proteins, NS I, NS2 and NS3/3A. NS I forms tubular structures and its function is currently unknown. To investigate the role of NS I in BTY infection, the interactions of NS I with mammalian and insect cellular proteins, and BTY viral proteins, were examined. BTY NS I was identi tied as interacting with aldolase A, NUBP 1, Pyruvate kinase M2, cathespin B, SUM 0-1 and peptide TY7 using the yeast two-hybrid system, ELISA and immunofluorescence analysis. TY7 and NS I caused extensive cell death within 24h of co-expression; this cell death was not apoptosis and reduced BTY yield by 37%. The interaction of NS I with SUMO-I and its importance in BTY infection was confinned using siRNA to knockdown SUMO-I during BTY-IO infection. Knockdown of SUMO-I elicited a dramatic reduction in virus yield by 73%. NS I interactions with proteins of the insect vector Culicoides were also examined. A putative interaction between NS 1 and the ubiquitin activating enzyme El (UBA EI) ofCulicoides was identified during screening of a phage library, this has not been confirmed by other means. NS 1 interactions with other BTY proteins were analysed using immunoprecipitation and a strong interaction between NS 1 and YP7 was identified; this was confim1ed using the yeast two-hybrid system and immunoflourescence. Two main roles have been hypothesised for NS I from this data; firstly it is likely that NS I interaction with SUMO-I and UBA E I allows the targeting of specific proteins for sumoylation and ubiquitination allowing NS 1 to modify the host response to BTY infection. Secondly it is possible that NS I serves as an anchor for YP7 and virus cores allowing the build up of cores at the cytoskeleton in close proximity to YP2 for subsequent assembly and release. RNAi against NS J eliminated tubule formation but did not affect virus yield or YP7 and SUMO-J distribution and expression. It is therefore likely that the function of NS I does not rely on tubule fom1ation and that tubules are a form of storage for the active monomer of NSI.
APA, Harvard, Vancouver, ISO, and other styles
5

Kamitani, Mari. "Analysis on virus-virus and virus-host interactions in Brassicaceae in natural environments." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225436.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Laidlaw, Stephen Mark. "Protein-protein interactions of fowlpox virus." Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.424671.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Ji, Xiaoyun. "Molecular interactions within insect virus polyhedra." Thesis, University of Oxford, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.540298.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Orthopoulos, George. "Coxsackie B virus host cell interactions." Thesis, University of Sussex, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419832.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Ratcliff, Frank Giles. "Novel aspects of plant-virus interactions." Thesis, University of East Anglia, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302040.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Bryden, Helen. "Host-virus interactions in Hodgkin's disease." Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.363166.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Virus interactions"

1

Bailer, Susanne M., and Diana Lieber, eds. Virus-Host Interactions. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-601-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kleinow, Tatjana, ed. Plant-Virus Interactions. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25489-0.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Aquino de Muro, Marilena, ed. Virus-Host Interactions. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2895-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Bailer, Susanne M., and Diana Lieber. Virus-host interactions: Methods and protocols. New York: Humana Press, 2013.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

S, Fraser R. S., ed. Recognition and response in plant-virus interactions. Berlin: Springer-Verlag, 1990.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

Fraser, Ron S. S., ed. Recognition and Response in Plant-Virus Interactions. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74164-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Doerfler, Walter, and Petra Böhm, eds. Adenoviruses: Model and Vectors in Virus-Host Interactions. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-662-05597-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Doerfler, Walter, and Petra Böhm, eds. Adenoviruses: Model and Vectors in Virus-Host Interactions. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-05599-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Edwards, Matthew J. Interactions of monoclonal antibodies with an influenza A virus. [s.l.]: typescript, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Billstrom, Marcella Anne. The interactions of concanavalin A and herpes simplex virus type 1: Application to virus purification. Birmingham: University of Birmingham, 1987.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Virus interactions"

1

Weischer, Bernhard. "Nematode-virus interactions." In Nematode Interactions, 217–31. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1488-2_10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Link, Katrin, and Uwe Sonnewald. "Interaction of Movement Proteins with Host Factors, Mechanism of Viral Host Cell Manipulation and Influence of MPs on Plant Growth and Development." In Plant-Virus Interactions, 1–37. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25489-0_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Heinlein, Manfred. "Viral Transport and Interaction with the Host Cytoskeleton." In Plant-Virus Interactions, 39–66. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25489-0_2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Love, Andrew J., Jane Shaw, and Michael E. Taliansky. "Virus-Induced Modification of Subnuclear Domain Functions." In Plant-Virus Interactions, 67–85. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25489-0_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Burch-Smith, Tessa M., and Patricia C. Zambryski. "Regulation of Plasmodesmal Transport and Modification of Plasmodesmata During Development and Following Infection by Viruses and Viral Proteins." In Plant-Virus Interactions, 87–122. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25489-0_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Ziebell, Heiko. "Plant Defence and Viral Interference." In Plant-Virus Interactions, 123–59. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25489-0_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Pooggin, Mikhail M. "Role of Small RNAs in Virus-Host Interaction." In Plant-Virus Interactions, 161–89. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-25489-0_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Yadav, Sunita, and Anju K. Chhibbar. "Plant–Virus Interactions." In Molecular Aspects of Plant-Pathogen Interaction, 43–77. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7371-7_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Yoshida, Takashi, Daichi Morimoto, and Shigeko Kimura. "Bacteria–Virus Interactions." In DNA Traffic in the Environment, 95–108. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-3411-5_5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Palukaitis, Peter, John P. Carr, and James E. Schoelz. "Plant–Virus Interactions." In Plant Virology Protocols, 3–19. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-102-4_1.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Virus interactions"

1

Lanchantin, Jack, Tom Weingarten, Arshdeep Sekhon, Clint Miller, and Yanjun Qi. "Transfer learning for predicting virus-host protein interactions for novel virus sequences." In BCB '21: 12th ACM International Conference on Bioinformatics, Computational Biology and Health Informatics. New York, NY, USA: ACM, 2021. http://dx.doi.org/10.1145/3459930.3469527.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Anglero-Rodriguez, Yesseinia. "Mosquito-fungus interactions enhance susceptibility to dengue virus." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.92976.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Taliansky, Michael E., Jane Shaw, Antonida Makhotenko, Andrew J. Love, Natalia O. Kalinina, and Stuart MacFarlane. "PLANT-VIRUS INTERACTIONS: THE ROLE OF SUBNUCLEAR STRUCTURES." In Viruses: Discovering Big in Small. TORUS PRESS, 2019. http://dx.doi.org/10.30826/viruses-2019-11.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Chisholm, Paul Joseph. "Competition with non-vectors mediates virus-vector interactions." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.115741.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Zarubaev, V., P. Anfimov, T. Krisko, A. Sirotkin, A. Kancer, E. Bykovskaya, A. Mayurova, et al. "Fullerene C60 and graphene photosensibiles for photodynamic virus inactivation." In Optical Interactions with Tissue and Cells XXIX, edited by E. Duco Jansen and Hope T. Beier. SPIE, 2018. http://dx.doi.org/10.1117/12.2294593.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Kolev, Mikhail K. "Mathematical modelling of the interactions between antibodies and virus." In 2008 Conference on Human System Interactions (HSI). IEEE, 2008. http://dx.doi.org/10.1109/hsi.2008.4581465.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Imler, Jean-Luc. "Host-virus interactions: Lessons from the model organismDrosophila melanogaster." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.92693.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Redinbaugh, Margaret (Peg). "Vector-virus interactions in maize agroecosystems in East Africa." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.94561.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Singh, Irtisha, Oznur Tastan, and Judith Klein-Seetharaman. "Comparison of virus interactions with human signal transduction pathways." In the First ACM International Conference. New York, New York, USA: ACM Press, 2010. http://dx.doi.org/10.1145/1854776.1854785.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Gammon, Don B. "Characterization of virus-lepidopteran host interactions using aLymantria disparmodel system." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.93814.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "Virus interactions"

1

Umland, Timothy C. Cross-Species Virus-Host Protein-Protein Interactions Inhibiting Innate Immunity. Fort Belvoir, VA: Defense Technical Information Center, July 2016. http://dx.doi.org/10.21236/ad1012633.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Ullman, Diane E., Benjamin Raccah, John Sherwood, Meir Klein, Yehezkiel Antignus, and Abed Gera. Tomato Spotted Wilt Tosporvirus and its Thrips Vectors: Epidemiology, Insect/Virus Interactions and Control. United States Department of Agriculture, November 1999. http://dx.doi.org/10.32747/1999.7573062.bard.

Full text
Abstract:
Objectives. The major aim of the proposed research was to study thrips-TSWV relationships and their role in the epidemiology of the virus with the aim of using this knowledge to reduce crop losses occurring due to epidemics. Our specific objectives were: To determine the major factors involved in virus outbreaks, including: a) identifying the thrips species involved in virus dissemination and their relative role in virus spread; b) determining the virus sources among wild and cultivated plants throughout the season and their role in virus spread, and, c) determining how temperature and molecular variations in isolates impact virus replication in plants and insects and impact the transmission cycle. Background to the topic. Tospoviruses are among the most important emerging plant viruses that impact production of agricultural and ornamental crops. Evolution of tospoviruses and their relationships with thrips vector species have been of great interest because of crop damage caused world wide and the complete absence of suitable methods of control. Tospoviruses threaten crops in Israel and the United States. By understanding the factors contributing to epidemics and the specific relationships between thrips species and particular tospoviruses we hope that new strategies for control can be developed that will benefit agriculture in both Israel and the United States. Major conclusions, solutions, achievements. We determined that at least three tospoviruses were involved in epidemics in Israel and the United States, tomato spotted wilt virus (TSWV), impatiens necrotic spot virus (INSV) and iris yellow spot virus (IYSV). We detected and characterized INSV for the first time in Israel and, through our efforts, IYSV was detected and characterized for the first time in both countries. We demonstrated that many thrips species were present in commercial production areas and trap color influenced thrips catch. Frankliniella occidentalis was the major vector species of INSV and TSWV and populations varied in transmission efficiency. Thrips tabaci is the sole known vector of IYSV and experiments in both countries indicated that F. occidentalis is not a vector of this new tospovirus. Alternate plant hosts were identified for each virus. A new monitoring system combining sticky cards and petunia indicator plants was developed to identify sources of infective thrips. This system has been highly successful in the U.S. and was used to demonstrate to growers that removal of plant sources of infective thrips has a dramatic impact on virus incidence. Finally, a putative thrips receptor mediating acquisition of TSWV was discovered. Implications, scientific and agricultural. Our findings have contributed to new control measures that will benefit agriculture. Identification of a putative thrips receptor for TSWV and our findings relative to thrips/tospovirus specificity have implications for development of innovative new control strategies.
APA, Harvard, Vancouver, ISO, and other styles
3

Palukaitis, Peter, Amit Gal-On, Milton Zaitlin, and Victor Gaba. Virus Synergy in Transgenic Plants. United States Department of Agriculture, March 2000. http://dx.doi.org/10.32747/2000.7573074.bard.

Full text
Abstract:
Transgenic plants expressing viral genes offer novel means of engendering resistance to those viruses. However, some viruses interact synergistically with other viruses and it is now known that transgenic plants expressing particular genes of one virus may also mediate synergy with a second virus. Thus, our specific objectives were to (1) determine if transgenic plants resistant to one virus showed synergy with another virus; (2) determine what viral sequences were essential for synergy; and (3) determine whether one of more mechanisms were involved i synergy. This project would also enable an evaluation of the risks of synergism associated with the use of such transgenic plants. The conclusion deriving from this project are as follows: - There is more than one mechanism of synergy. - The CMV 2b gene is required for synergistic interactions. - Synergy between a potyvirus and CMV can break natural resistance limiting CMV movement. - Synergy operates at two levels - increase in virus accumulation and increase in pathology - independently of each other. - Various sequences of CMV can interact with the host to alter pathogenicity and affect virus accumulation. - The effect of synergy on CMV satellite RNA accumulatio varies in different systems. - The HC-Pro gene may only function in host plant species to induce synergy. - The HC-Pro is a host range determinant of potyviruses. - Transgenic plants expressing some viral sequences showed synergy with one or more viruses. Transgenic plants expressing CMV RNA 1, PVY NIb and the TMV 30K gene all showed synergy with at least one unrelated virus. - Transgenic plants expressing some viral sequences showed interference with the infection of unrelated viruses. Transgenic plants expressing the TMV 30K, 54K and 126K genes, the PVY NIb gene, or the CMV 3a gene all showed some level of interference with the accumulation (and in some cases the pathology) of unrelated viruses. From our observations, there are agricultural implications to the above conclusions. It is apparent that before they are released commercially, transgenic plants expressing viral sequences for resistance to one virus need to be evaluated fro two properties: - Synergism to unrelated viruses that infect the same plant. Most of these evaluations can be made in the greenhouse, and many can be predicted from the known literature of viruses known to interact with each other. In other cases, where transgenic plants are being generated from new plant species, the main corresponding viruses from the same known interacting genera (e.g., potexviruses and cucumoviruses, potyviruses and cucumoviruses, tobamoviruses and potexviruses, etc.) should be evaluated. - Inhibition or enhancement of other resistance genes. Although it is unlikely that plants to be released would be transformed with HC-Pro or 2b genes, there may be other viral genes that can affect the expression of plant genes encoding resistance to other pathogens. Therefore, transgenic plants expressing viral genes to engender pathogen-derived resistance should be evaluated against a spectrum of other pathogens, to determine whether those resistance activities are still present, have been lost, or have been enhanced!
APA, Harvard, Vancouver, ISO, and other styles
4

Davidson, Irit, Hsing-Jien Kung, and Richard L. Witter. Molecular Interactions between Herpes and Retroviruses in Dually Infected Chickens and Turkeys. United States Department of Agriculture, January 2002. http://dx.doi.org/10.32747/2002.7575275.bard.

Full text
Abstract:
Tumors in commercial poultry are caused mainly by infection with avian herpes and retroviruses, the herpesvirus Marek's disease virus (MDV) and the retroviruses, reticuloendotheliosis (REV), lymphoid leukosis, subgroups A-I and J (ALV and ALV-J) in chickens, or Iymphoprolipherative disease (LPDV) in turkeys. Infection with one virus aggravates the clinical outcome of birds that are already infected by another oncogenic virus. As these viruses do not interfere for infection, MDV and one or more retroviruses can infect the same flock, the same bird and the same cell. While infecting the same cell, herpes and retroviruses might interact in at least three ways: a) Integration of retrovirus genomes, or genomic fragments (mainly the LTR) into MDV;b) alteration of LTR-driven expression of retroviral genes by MDV immediate- early genes, and c) by herpesvirus induced cellular transcriptional factors. The first type of molecular interaction have been demonstrated to happen efficiently in vitro by Dr. Kung, in cases multiple infection of cell cultures with MDV and REV or MDV and ALV. Moreover, Dr. Witter showed that an in vitro-created recombinant, RM1, had altered in vitro replication and in vivo biological properties. A more comprehensive characterization of RM1 was carried out in the present project. We sought to highlight whether events of such integrations occur also in the bird, in vivo. For that, we had first to determine the prevalence of dually-infected individual birds in commercial flocks, as no systematic survey has been yet reported. Surprisingly, about 25% of the commercial flocks infected with avian oncogenic viruses had a multiple virus infection and 5% of the total samples ana lysed had multiple virus sequences. Then, we aimed to evaluate and characterize biologically and molecularly the resulting recombinants, if formed, and to analyse the factors that affect these events (virus strains, type and age of birds and time interval between the infection with both viruses). The perception of retrovirus insertions into herpesviruses in vivo is not banal, as the in vivo and in vitro systems differ in the viral-target cells, lymphocytes or fibroblasts, in the MDV-replicative type, transforming or productive, and the immune system presence. We realized that previous methods employed to study in vitro created recombinant viruses were not adequate for the study of samples taken directly from the bird. Therefore, the Hot Spot-combined PCR was developed based on the molecularly known RM1 virus. Also, the PFGE that was used for tissue cultured-MDV separation was inefficient for separating MDV from organs, but useful with feather tips as a source of bird original MDV. Much attention was dedicated now to feathers, because if a recombinant virus would be formed in vivo, its biological significance would be evident by horizontal dissemination through the feathers. Major findings were: a) not only in vitro, but also in vivo MDV and retrovirus co-infections lead to LTR integrations into MDV. That was shown by the detection of chimeric molecules. These appeared in low quantities and as quasispecies, thus interfering with sequence analysis of cloned gel-purified chimeric molecules. Mainly inserts were located in the repeat long MDV fragments. In field birds chimeric molecules were detected at a lower frequency (2.5%) than in experimentally infected birds (30-50%). These could be transmitted experimentally to another birds by inoculation with chimeric molecules containing blood. Several types of chimeric molecules were formed, and same types were detected in birds infected by a second round. To reproduce viral integrations, in vivo infection trials were done with field inoculate that contained both viruses, but the chimeric molecule yield was undetectable.
APA, Harvard, Vancouver, ISO, and other styles
5

Valverde, Rodrigo A., Aviv Dombrovsky, and Noa Sela. Interactions between Bell pepper endornavirus and acute viruses in bell pepper and effect to the host. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598166.bard.

Full text
Abstract:
Based on the type of relationship with the host, plant viruses can be grouped as acute or persistent. Acute viruses are well studied and cause disease. In contrast, persistent viruses do not appear to affect the phenotype of the host. The genus Endornavirus contains persistent viruses that infect plants without causing visible symptoms. Infections by endornaviruses have been reported in many economically important crops, such as avocado, barley, common bean, melon, pepper, and rice. However, little is known about the effect they have on their plant hosts. The long term objective of the proposed project is to elucidate the nature of the symbiotic interaction between Bell pepper endornavirus (BPEV) and its host. The specific objectives include: a) to evaluate the phenotype and fruit yield of endornavirus-free and endornavirus-infected bell pepper near-isogenic lines under greenhouse conditions; b) to conduct gene expression studies using endornavirus-free and endornavirus-infected bell pepper near-isogenic lines; and c) to study the interactions between acute viruses, Cucumber mosaic virus Potato virus Y, Pepper yellow leaf curl virus, and Tobacco etch virus and Bell pepper endornavirus. It is likely that BPEV in bell pepper is in a mutualistic relationship with the plant and provide protection to unknown biotic or abiotic agents. Nevertheless, it is also possible that the endornavirus could interact synergistically with acute viruses and indirectly or directly cause harmful effects. In any case, the information that will be obtained with this investigation is relevant to BARD’s mission since it is related to the protection of plants against biotic stresses.
APA, Harvard, Vancouver, ISO, and other styles
6

Schat, Karel Antoni, Irit Davidson, and Dan Heller. Chicken infectious anemia virus: immunosuppression, transmission and impact on other diseases. United States Department of Agriculture, 2008. http://dx.doi.org/10.32747/2008.7695591.bard.

Full text
Abstract:
1. Original Objectives. The original broad objectives of the grant were to determine A) the impact of CAV on the generation of cytotoxic T lymphocytes (CTL) to reticuloendotheliosis virus (REV) (CU), B). the interactions between chicken anemia virus (CAV) and Marek’s disease virus (MDV) with an emphasis on horizontal spread of CAV through feathers (KVI), and C) the impact of CAV infection on Salmonella typhimurium (STM) (HUJI). During the third year and the one year no cost extension the CU group included some work on the development of an antigen-antibody complex vaccine for CAV, which was partially funded by the US Poultry and Egg Association. 2. Background to the topic. CAV is a major pathogen causing clinical disease if maternal antibody-free chickens are infected vertically or horizontally between 1 and 14 days of age. Infection after 3 weeks of age when maternal antibodies are not longer present can cause severe subclinical immunosuppression affecting CTL and cytokine expression. The subclinical immunosuppression can aggravate many diseases including Marek’s disease (MD) and several bacterial infections. 3. Major conclusions and achievements. The overall project contributed in the following ways to the knowledge about CAV infection in poultry. As expected CAV infections occur frequently in Israel causing problems to the industry. To control subclinical infections vaccination may be needed and our work indicates that the development of an antigen-antibody complex vaccine is feasible. It was previously known that CAV can spread vertically and horizontally, but the exact routes of the latter had not been confirmed. Our results clearly show that CAV can be shed into the environment through feathers. A potential interaction between CAV and MD virus (MDV) in the feathers was noted which may interfere with MDV replication. It was also learned that inoculation of 7-day-old embryos causes growth retardation and lesions. The potential of CAV to cause immunosuppression was further examined using CTL responses to REV. CTL were obtained from chickens between 36 and 44 days of age with REV and CAV given at different time points. In contrast to our earlier studies, in these experiments we were unable to detect a direct impact of CAV on REV-specific CTL, perhaps because the CTL were obtained from older birds. Inoculation of CAV at one day of age decreased the IgG antibody responses to inactivated STM administered at 10 days of age. 4. Scientific and Agricultural Implications The impact of the research was especially important for the poultry industry in Israel. The producers have been educated on the importance of the disease through the many presentations. It is now well known to the stakeholders that CAV can aggravate other diseases, decrease productivity and profitability. As a consequence they monitor the antibody status of the breeders so that the maternal antibody status of the broilers is known. Also vaccination of breeder flock that remain antibody negative may become feasible further reducing the negative impact of CAV infection. Vaccination may become more important because improved biosecurity of the breeder flocks to prevent avian influenza and Salmonella may delay the onset of seroconversion for CAV by natural exposure resulting in CAV susceptible broilers lacking maternal antibodies. Scientifically, the research added important information on the horizontal spread of CAV through feathers, the interactions with Salmonella typhimurium and the demonstration that antigen-antibody complex vaccines may provide protective immunity.
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
9

Gafni, Yedidya, and Vitaly Citovsky. Inactivation of SGS3 as Molecular Basis for RNA Silencing Suppression by TYLCV V2. United States Department of Agriculture, November 2013. http://dx.doi.org/10.32747/2013.7593402.bard.

Full text
Abstract:
The Israeli isolate of Tomato yellow leaf curl geminivirus(TYLCV-Is) is a major tomato pathogen, causing extensive crop losses in Israel and in the south-eastern U.S. Yet, little is known about the molecular mechanisms of its interaction with tomato cells. One of the most interesting aspects of such interaction is how the invading virus counteracts the RNA silencing response of the plant. In the former BARD project, we have shown that TYLCV-Is V2 protein is an RNA silencing suppressor, and that this suppression is carried out via the interaction of V2 with the SGS3 component of the plant RNA silencing machinery. This reported project was meant to use our data as a foundation to elucidate the molecular mechanism by which V2 affects the SGS3 activity. While this research is likely to have an important impact on our understanding of basic biology of virus-plant interactions and suppression of plant immunity, it also will have practical implications, helping to conceive novel strategies for crop resistance to TYLCV-Is. Our preliminary data in regard to V2 activities and our present knowledge of the SGS3 function suggest likely mechanisms for the inhibitory effect of V2 on SGS3. We have shown that V2 possess structural and functional hallmarks of an F-box protein, suggesting that it may target SGS3 for proteasomal degradation. SGS3 contains an RNA-binding domain and likely functions to protect the cleavage produces of the primary transcript for subsequent conversion to double-stranded forms; thus, V2 may simply block the RNA binding activity of SGS3. V2 may also employ a combination of these mechanisms. These and other possibilities were tested in this reported project.
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Virus interactions' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography