Relevant bibliographies by topics / Influenza virus

Academic literature on the topic 'Influenza virus'

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Published: 4 June 2021
Last updated: 22 June 2024

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Journal articles on the topic "Influenza virus"

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Arbo, Antonio. "Influenza: the changing virus." Revista del Instituto de Medicina Tropical 12, no. 2 (December 30, 2017): 1–2. http://dx.doi.org/10.18004/imt/20171221-2.

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Juozapaitis, Mindaugas, and Linas Antoniukas. "Influenza virus." Medicina 43, no. 12 (December 8, 2007): 919. http://dx.doi.org/10.3390/medicina43120119.

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Every year, especially during the cold season, many people catch an acute respiratory disease, namely flu. It is easy to catch this disease; therefore, it spreads very rapidly and often becomes an epidemic or a global pandemic. Airway inflammation and other body ailments, which form in a very short period, torment the patient several weeks. After that, the symptoms of the disease usually disappear as quickly as they emerged. The great epidemics of flu have rather unique characteristics; therefore, it is possible to identify descriptions of such epidemics in historic sources. Already in the 4th century BC, Hippocrates himself wrote about one of them. It is known now that flu epidemics emerge rather frequently, but there are no regular intervals between those events. The epidemics can differ in their consequences, but usually they cause an increased mortality of elderly people. The great flu epidemics of the last century took millions of human lives. In 1918–19, during “The Spanish” pandemic of flu, there were around 40–50 millions of deaths all over the world; “Pandemic of Asia” in 1957 took up to one million lives, etc. Influenza virus can cause various disorders of the respiratory system: from mild inflammations of upper airways to acute pneumonia that finally results in the patient’s death. Scientist Richard E. Shope, who investigated swine flu in 1920, had a suspicion that the cause of this disease might be a virus. Already in 1933, scientists from the National Institute for Medical Research in London – Wilson Smith, Sir Christopher Andrewes, and Sir Patrick Laidlaw – for the first time isolated the virus, which caused human flu. Then scientific community started the exhaustive research of influenza virus, and the great interest in this virus and its unique features is still active even today.
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Hutchinson, Edward C. "Influenza Virus." Trends in Microbiology 26, no. 9 (September 2018): 809–10. http://dx.doi.org/10.1016/j.tim.2018.05.013.

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Freymuth, François. "Virus influenza." EMC - Biologie Médicale 1, no. 1 (January 2006): 1–9. http://dx.doi.org/10.1016/s2211-9698(06)76378-6.

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Cottey, Robert, Cheryl A. Rowe, and Bradley S. Bender. "Influenza Virus." Current Protocols in Immunology 42, no. 1 (April 2001): 19.11.1–19.11.32. http://dx.doi.org/10.1002/0471142735.im1911s42.

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&NA;. "Influenza virus vaccine/influenza A virus vaccine-H1N1." Reactions Weekly &NA;, no. 1382 (December 2011): 24–25. http://dx.doi.org/10.2165/00128415-201113820-00085.

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&NA;. "Influenza A virus vaccine-H1N1/influenza virus vaccine." Reactions Weekly &NA;, no. 1402 (May 2012): 29. http://dx.doi.org/10.2165/00128415-201214020-00104.

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&NA;. "Influenza A virus vaccine-H1N1/influenza virus vaccine." Reactions Weekly &NA;, no. 1313 (August 2010): 27. http://dx.doi.org/10.2165/00128415-201013130-00094.

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&NA;. "Influenza virus vaccine/influenza A virus vaccine H1N1." Reactions Weekly &NA;, no. 1329 (November 2010): 23. http://dx.doi.org/10.2165/00128415-201013290-00076.

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&NA;. "Influenza A virus vaccine H1N1/influenza virus vaccine." Reactions Weekly &NA;, no. 1332 (December 2010): 24–25. http://dx.doi.org/10.2165/00128415-201013320-00080.

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Dissertations / Theses on the topic "Influenza virus"

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Höfer, Chris Tina. "Influenza virus assembly." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17251.

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Influenza A Viren besitzen ein segmentiertes, einzelsträngiges RNA-Genom, welches in Form viraler Ribonukleoprotein (vRNP)-Komplexe verpackt ist. Während das virale Genom im Zellkern repliziert wird, finden Assemblierung und Knospung reifer Viruspartikel an der apikalen Plasmamembran statt. Für die Virusbildung müssen die einzelnen viralen Komponenten hierher gebracht werden. Während intrinsische apikale Signale der viralen Transmembranproteine bekannt sind, sind der zielgerichtete Transport und der Einbau des viralen Genoms in neuentstehende Virionen noch wenig verstanden. In dieser Arbeit wurden potentielle Mechanismen des vRNP-Transportes untersucht, wie die Fähigkeit der vRNPs mit Lipidmembranen zu assoziieren und die intrinsische subzellulären Lokalisation des viralen Nukleoproteins (NP), eines Hauptbestandteils der vRNPs. Es konnte gezeigt werden, dass vRNPs nicht mit Lipidmembranen assoziieren, was mittels Flotation aufgereinigter vRNPs mit Liposomen unterschiedlicher Zusammensetzung untersucht wurde. Die Ergebnisse deuten jedoch darauf hin, dass das virale M1 in der Lage ist, Bindung von vRNPs an negativ-geladene Lipidmembranen zu vermitteln. Subzelluläre Lokalisation von NP wurde des Weiteren durch Expression fluoreszierender NP-Fusionsproteine und Fluoreszenzphotoaktivierung untersucht. Es konnte gezeigt werden, dass NP allein nicht mit zytoplasmatischen Strukturen assoziiert, stattdessen aber umfangreiche Interaktionen im Zellkern eingeht und mit hoher Affinität mit bestimmten Kerndomänen assoziiert, und zwar den Nukleoli sowie kleinen Kerndomänen, welche häufig in der Nähe von Cajal-Körperchen und PML-Körperchen zu finden waren. Schließlich wurde ein experimenteller Ansatz etabliert, welcher erlaubt, den Transport vRNP-ähnlicher Komplexe mittels Fluoreszenzdetektion aufzuzeichnen und Einzelpartikelverfolgungsanalysen durchzuführen. Unterschiedliche Phasen des vRNP-Transportes konnten beobachtet werden und ein 3-Phasen-Transportmodell wird skizziert.
Influenza A viruses have a segmented single-stranded RNA genome, which is packed in form of viral ribonucleoprotein (vRNP) complexes. While the viral genome is replicated and transcribed in the host cell nucleus, assembly and budding of mature virus particles take place at the apical plasma membrane. Efficient virus formation requires delivery of all viral components to this site. While intrinsic apical targeting signals of the viral transmembrane proteins have been identified, it still remains poorly understood how the viral genome is transported and targeted into progeny virus particles. In this study, potential targeting mechanisms were investigated like the ability of vRNPs to associate with lipid membranes and the intrinsic ability of the viral nucleoprotein (NP) – which is the major protein component of vRNPs – for subcellular targeting. It could be shown that vRNPs are not able to associate with model membranes in vitro, which was demonstrated by flotation of purified vRNPs with liposomes of different lipid compositions. Results indicated, however, that the matrix protein M1 can mediate binding of vRNPs to negatively charged lipid bilayers. Intrinsic subcellular targeting of NP was further investigated by expression of fluorescent NP fusion protein and fluorescence photoactivation, revealing that NP by itself does not target cytoplasmic structures. It was found to interact extensively with the nuclear compartment instead and to target specific nuclear domains with high affinity, in particular nucleoli and small interchromatin domains that frequently localized in close proximity to Cajal bodies and PML bodies. An experimental approach was finally established that allowed monitoring the transport of vRNP-like complexes in living infected cells by fluorescence detection. It was possible to perform single particle tracking and to describe different stages of vRNP transport between the nucleus and the plasma membrane. A model of three-stage transport is suggested.
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Mittelholzer, Camilla Maria. "Influenza virus - protection and adaptation /." Stockholm, 2006. http://diss.kib.ki.se/2006/91-7140-656-5/.

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Green, P. C. "Serological and immunocytochemical studies on influenza virus and influenza virus infected cells." Thesis, University of Manchester, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356114.

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Wallensten, Anders. "Influenza A virus in wild birds." Doctoral thesis, Linköping : Linköping University, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-7643.

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Morgan, David John. "Defective interfering influenza virus reverses the immunopathological effects of standard influenza virus in mice." Thesis, University of Bristol, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332491.

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Seekings, Amanda Hanna. "Emergence of H7 highly pathogenic avian influenza virus from low pathogenicity avian influenza virus." Thesis, Imperial College London, 2017. http://hdl.handle.net/10044/1/52910.

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Outbreaks of highly pathogenic avian influenza virus (HPAIV) may result in the infection of millions of poultry, causing devastating disease and up to 100% mortality. Avian influenza outbreaks and laboratory experiments have shown that HPAIV can emerge from low pathogenicity avian influenza virus (LPAIV) precursors. The multi-basic cleavage site (MBCS) in the haemagglutinin protein is described as the main pathogenic determinant of HPAIV infection in poultry. Identifying a precursor LPAIV is important for understanding the molecular changes involved in the emergence of HPAIV. In 2008, H7N7 HPAIV was confirmed in Oxfordshire, UK. The presence of a LPAIV precursor with a rare di-basic cleavage site (DBCS) was identified. The DBCS contains an additional basic amino acid compared to common circulating LPAIVs that harbour a single basic amino acid at the cleavage site (SBCS). Using reverse genetics, isogenic viruses based on A/chicken/England/11406/2008 H7N7 HPAIV, from the outbreak, were rescued with the MBCS replaced with either a DBCS (H7N7DB) as seen in the putative LPAIV precursor or a SBCS representative of common H7 LPAIVs (H7N7SB). Intravenous pathogenicity index testing of the recombinant viruses confirmed that only the MBCS conferred the highly pathogenic phenotype. Following passage in ovo, H7N7DB showed evidence of spontaneous evolution to a HPAIV genotype and phenotype as demonstrated by the acquisition of a MBCS, and by influenza virus-specific immunohistochemistry staining in embryo vascular endothelial cells. In contrast, deep sequencing of tissues from embryos in which H7N7SB was serially passaged up to three times showed retention of the LPAIV genotype. Thus, in chicken embryos, an H7N7 virus containing a DBCS displays an unstable nature allowing for rapid evolution to HPAIV. In ovo passage presents a novel approach to assess the likelihood of a LPAIV to evolve into HPAIV, and allows a laboratory-based dissection of molecular mechanisms behind the emergence of HPAIV.
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Jia, Nan. "Glycobiology studies of influenza virus." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/50787.

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Glycans represent a class of macromolecules that exhibit vital biological roles in living organisms. They are not only essential for maintaining the normal functionalities of a cell, but are also involved in many pathogenic processes. The influenza A virus binds to glycan receptors that are expressed on the surface of respiratory epithelial cells of human airway and thereby initiates infection. Deciphering the structural features of glycans and comprehending their functional implications are thus crucial to expand our understandings of the disease. To validate the alternative models that are used in the studies of influenza, we generated the glycomic profiles from in vivo and in vitro experimental systems by mass spectrometry. A combination of MALDI-TOF MS, MALDI-TOF-TOF MS/MS, GC-EI-MS and enzymatic digestion experiments were utilised to characterise the structure of glycans. The ferret has been used as an experimental animal to investigate the transmission and replication of influenza viruses. To verify the validity of this model, we carried out glycomic characterisation of ferret respiratory tissues to complement the data that was generated from human airway tissues. The mass spectrometric analysis indicates that the respiratory glycosylation of ferret highly resembles that of human, although distinctive expression of glycans displaying the Sda epitope are detected exclusively in ferret. Nonetheless, in comparison to other lab animals such as mouse and swine, ferret remains a better alternative model for studying the pathogenicity of influenza viruses. In the second project, we generated the glycomic profiles from human and ferret respiratory epithelial cells that were cultured under experimental conditions. Glycosylation patterns between these two in vitro systems are largely comparable, except the presence of the Sda epitope in ferret cells. However, when compared to their corresponding in vivo tissues, diminished structural repertoires especially the high-mass structures were observed.
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Read, Eliot Keith Curtis. "Investigating influenza A virus RNA trafficking." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609127.

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Tan, E.-Pien. "Screening for influenza virus resistance genes." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608229.

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Kudryavtseva, Katerine. "Genome packaging in influenza A virus." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648592.

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Books on the topic "Influenza virus"

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Kawaoka, Yoshihiro, and Gabriele Neumann, eds. Influenza Virus. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-621-0.

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Yamauchi, Yohei, ed. Influenza Virus. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8678-1.

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Spackman, Erica, ed. Animal Influenza Virus. New York, NY: Springer US, 2020. http://dx.doi.org/10.1007/978-1-0716-0346-8.

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Spackman, Erica, ed. Avian Influenza Virus. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-279-3.

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Spackman, Erica, ed. Animal Influenza Virus. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-0758-8.

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Animal influenza virus. New York: Humana Press, 2014.

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Erica, Spackman, ed. Avian influenza virus. Totowa, NJ: Humana Press, 2008.

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Influenza virus: Methods and protocols. New York: Humana, 2012.

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Morgan, David John. Dejective interfering influenza virus reverses the immunopathological effects of standard influenza virus in mice. [s.l.]: typescript, 1992.

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von Itzstein, Mark, ed. Influenza Virus Sialidase - A Drug Discovery Target. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-7643-8927-7.

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Book chapters on the topic "Influenza virus"

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Suarez, David L. "Influenza A virus." In Animal Influenza, 1–30. Hoboken, NJ, USA: John Wiley & Sons, Inc., 2016. http://dx.doi.org/10.1002/9781118924341.ch1.

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Zinserling, Vsevolod A., and Vladimir A. Dedov. "Influenza Virus." In Infectious Disease and Parasites, 179–82. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-30009-2_1042.

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Kradin, Richard L., and Jay A. Fishman. "Influenza Virus." In Viruses and the Lung, 79–86. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-40605-8_9.

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Klenk, Hans Dieter. "Influenza-Virus." In Lexikon der Infektionskrankheiten des Menschen, 441–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-39026-8_512.

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Shahab, Shamsa Z., and W. Paul Glezen. "Influenza Virus." In Clinical Perspectives in Obstetrics and Gynecology, 215–23. New York, NY: Springer New York, 1994. http://dx.doi.org/10.1007/978-1-4612-2640-6_12.

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Hayden, Frederick G., and Peter Palese. "Influenza Virus." In Clinical Virology, 1009–58. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555819439.ch43.

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Matsubara, Teruhiko, and Toshinori Sato. "Influenza Virus." In Diamond Electrodes, 237–48. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-7834-9_15.

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Lydyard, Peter M., Michael F. Cole, John Holton, William L. Irving, Nina Porakishvili, Pradhib Venkatesan, and Katherine N. Ward. "Influenza virus." In Case Studies in Infectious Disease, 181–91. 2nd ed. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003155447-19.

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Spackman, Erica. "A Brief Introduction to the Avian Influenza Virus." In Avian Influenza Virus, 1–6. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-279-3_1.

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Pantin-Jackwood, Mary J. "Immunohistochemical Staining for the Detection of the Avian Influenza Virus in Tissues." In Avian Influenza Virus, 77–83. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-279-3_10.

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Conference papers on the topic "Influenza virus"

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Zabrodskaya, Y. A., N. V. Gavrilova, M. A. Plotnikova, and A. A. Lozhkov. "THE INFLUENCE OF EXOSOMES SECRETED BY BOTH INFLUENZA VIRUS-INFECTED AND NON-INFECTED CELLS ON VIRUS REPLICATION." In OpenBio-2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-247.

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Exosomes secreted by both influenza virus infected (EV) and non-infected (E) cells were isolated. It was demonstrated that EVs could suppress the immune response of cells. When cells were infected with the influenza virus in the presence of either E or EV, it was observed that E had a protective effect, reducing virus replication. Conversely, EV had a proviral effect, meaning it enhanced virus replication.
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Sharabrin, S. V., M. B. Borgoyakova, E. V. Starostina, D. N. Kisakov, L. A. Kisakova, S. I. Krasnikova, A. S. Gudymo, et al. "EXPERIMENTAL MRNA VACCINE AGAINST H1N1 INFLUENZA VIRUS." In X Международная конференция молодых ученых: биоинформатиков, биотехнологов, биофизиков, вирусологов и молекулярных биологов — 2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-393.

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The work is devoted to the development of an experimental mRNA vaccine encoding H1N1 influenza virus hemagglutinin and containing the β-globin sequence as 5’- and 3’-untranslated regions. Immunization of BALB/C mice caused the induction of specific antibodies with virus-neutralizing activity, forms a T-cell immune response, and provided 60 % protection of animals from lethal infection with the H1N1 influenza virus.
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Srinivasan, Balaji, Husein Rokadia, Steve Tung, Ronghui Wang, and Yanbin Li. "AFM Investigation of Avian Influenza Viruses." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-38952.

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The present paper describes a direct label-free diagnostic method that uses atomic force microscopy (AFM) to identify avian influenza virus strains through their electrical properties. In this method, a single virus particle is sandwiched between a rigid, conductive substrate and a conductive AFM tip (radius ∼ 8nm). Electrical characterization is achieved by probing the complex impedance spectrum of the sandwiched virus while mechanical characterization is achieved through nanoindentation. A total of three virus strains (inactivated) with different combinations of glycoprotein subtypes (H2N2, H3N5 and H4N6) were tested. Results from the electrical characterization indicate that the impedance spectra of different virus strains are indeed different. While the average electrical capacitance of a virus particle is about 17pF, the variation from one strain to another can be as high as 70%. A COMSOL Multiphysics™ simulation was carried out to estimate the electrical properties of the glycoproteins on the virus particle by comparing the simulated capacitance to the experimentally obtained values. The result indicates that the electrical conductivity of the glycoproteins is in the range of 9 to 14 mS and the dielectric constant value is around 2. The present results strongly suggest the possibility of using AFM as a diagnostic tool for direct recognition of avian influenza virus strains.
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Gavrilova, N. V., V. V. Vysochinskaya, E. A. Elpaeva, O. A. Dobrovolskaya, M. A. Plotnikova, A. A. Lozhkov, E. L. Zimmerman, A. A. Shaldzhyan, and Y. A. Zabrodskaya. "ANTIVIRAL ACTIVITY OF MRNAS ENCODING ANTIBODIES, TARGETING INFLUENZA A HEMAGGLUTININ AND INFLUENZA B NUCLEOPROTEIN IN VITRO." In OpenBio-2023. Novosibirsk State University, 2023. http://dx.doi.org/10.25205/978-5-4437-1526-1-239.

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Influenza poses a significant public health concern, and the development of therapeutic antibodies provides a promising avenue for its treatment. In this study, we generated mRNA sequences encoding neutralizing antibodies targeting the hemagglutinin of influenza A virus, as well as antibodies specific to the nucleoprotein of influenza B virus. We successfully demonstrated the antiviral activity of mRNA-encoded antibodies targeting the hemagglutinin against influenza A virus in vitro.
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Ejima, Miho, Keiko Haraguchi, Tadashi Yamamoto, and Ayae Honda. "Effect of PB1c45 on Influenza Virus Replication." In 2006 IEEE International Symposium on MicroNanoMechanical and Human Science. IEEE, 2006. http://dx.doi.org/10.1109/mhs.2006.320241.

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Ueda, Ryuta, Akihiko Ichkawa, Mariko Kusunoki, Miho Ejima, Fumito Arai, Toshio Fukuda, and Ayae Honda. "Influenza virus selects cell phase for infection." In 2007 International Symposium on Micro-NanoMechatronics and Human Science. IEEE, 2007. http://dx.doi.org/10.1109/mhs.2007.4420821.

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Lee, Dongjin, Yogesh Chander, Sagar M. Goyal, and Tianhong Cui. "Carbon Nanotubes Swine Influenza (H1N1) Virus Sensors." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-40735.

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We present a label-free detection of swine influenza virus (SIV) H1N1 by means of the excellent electrical properties of single-walled carbon nanotubes (SWCNTs). The electrical resistance of SWCNT resistor tends to increase upon the surface adsorption of macromolecules such as poly-L-lysine, anti-SIV antibodies, and SIVs in the process of immunoassay. The SWCNT network resistor was successfully able to detect as low as 180 TCID50/ml of SIV using the resistance shifts upon immunobinding of SIVs. The sensor specificity was demonstrated against transmissible gastroenteritis virus (TGEV) and feline calicivirus (FCV). This facile CNT-based immnoassay has potential applications as a rapid point-of-care detection or a sensing platform for lab-on-a-chip systems.
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Mehrbod, Parvaneh, Aini Ideris, Abdul Rahman Omar, and Mohd Hair Bejo. "Statins as antiviral drugs against influenza virus." In 3rd Annual International Conference on Advances in Biotechnology (BioTech 2013). Global Science and Technology Forum, 2013. http://dx.doi.org/10.5176/2251-2489_biotech13.70.

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Marriott, HM, MK Whyte, and DH Dockrell. "Macrophage Apoptosis after Influenza A Virus Infection." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5168.

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Pongsumpun, Puntani. "Local Stability of Influenza Virus with Vaccination." In ICISDM 2020: 2020 the 4th International Conference on Information System and Data Mining. New York, NY, USA: ACM, 2020. http://dx.doi.org/10.1145/3404663.3404684.

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Reports on the topic "Influenza virus"

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Perk, Shimon, Maricarmen Garcia, Alexander Panshin, Caroline Banet-Noach, Irina Gissin, Mark W. Jackwood, and David Stallknecht. Avian Influenza Virus H9N2: Characterization and Control Strategies. United States Department of Agriculture, June 2007. http://dx.doi.org/10.32747/2007.7709882.bard.

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Control of Avian Influenza (AI) infection is a highly topical subject of major economicimportance for the worldwide poultry industry at the national level and for international trade.H9N2 viruses are endemic in poultry throughout Asia and the Middle East, causing major losses inproduction. Moreover, these viruses pose wider threats since they have been isolated from bothswine and humans. At the same time, study of the AI viruses affords an opportunity to explore anumber of problems of intriguing scientific interest. The overall goal of this project was to developa sound control strategy for avian influenza subtype H9N2 viruses (AI H9N2) in commercialpoultry in Israel. The one-year feasibility study focused on two main goals, namely: to study themolecular characteristics of AI H9N2 circulating during the last seven years in Israel and todevelop tools enabling differentiation between the immune response to vaccination and infectionwith H9N2.Genetic and phylogenetic characterization of 29 selected AI H9N2 isolates (2000-2006)was performed by complete sequencing of hemagglutinin (HA), neuraminidase (NA), and all sixinternal genes [nucleoprotein (NP), polymerase basic 1 (PB1), polymerase basic 2 (PB2),polymerase acid (PA), matrix (M), and nonstructural (NS) genes]; comparative phylogenetic andgenetic analyses of these sequences; and comparative genetic analyses of deduced amino acidsequences of the HA, NA, NS1, and NS2 proteins. The major conclusions of the molecularanalyses were: (1) Israeli isolates, together with other H9N2 viruses isolated in Middle Eastcountries, comprise a single regional sublineage related to the G1-lineage. In addition, Israeliisolates subdivided into three different subgroups. Genetic analysis of these viruses suggests thatthey underwent divergent evolution paths.
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Dimitrova, Adriana, Milka Mileva, Dimo Krastev, Ivan Kindekov, and Angel G. Galabov. Multiorgan Pathological Changes Caused by Experimental Influenza Virus Infection in Mice. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, October 2021. http://dx.doi.org/10.7546/crabs.2021.10.07.

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Perk, Simon, Egbert Mundt, Alexander Panshin, Irit Davidson, Irina Shkoda, Ameera AlTori, and Maricarmen Garcia. Characterization and Control Strategies of Low Pathogenic Avian Influenza Virus H9N2. United States Department of Agriculture, November 2012. http://dx.doi.org/10.32747/2012.7697117.bard.

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The avian influenza virus, subtype H9N2 subtype, defined as having a low pathogenicity, causes extensive economical losses in commercial flocks, probably due to management and synergism with other pathogens. AIV H9N2 was first identified in Israel in the year 2000, and since then it became endemic and widespread in Israel. Control by vaccination of commercial flocks with an inactivated vaccine has been introduced since 2007. In face of the continuous H9N2 outbreaks, and the application of the vaccination policy, we aimed in the present study to provide a method of differentiating naturally infected from vaccinated animals (DIVA). The aim of the assay would be detect only antibodies created by a de-novo infection, since the inactivated vaccine virus is not reproducing, and might provide a simple tool for mass detection of novel infections of commercial flocks. To fulfill the overall aim, the project was designed to include four operational objectives: 1. Evaluation of the genetic evolution of AIV in Israel; 2. Assessment of the diagnostic value of an NS1 ELISA; 3. NS1 ELISA as evaluation criteria for measuring the efficacy of vaccination against H9N2 AIV; 4. Development of an AIV H9 subtype specific ELISA systems. Major conclusion and implications drawn from the project were: 1. A continuous genetic change occurred in the collection of H9N2 isolates, and new introductions were identified. It was shown thatthe differences between the HA proteins of viruses used for vaccine productionand local fieldisolatesincreasedin parallelwith the durationand intensity ofvaccine use, therefore, developing a differential assay for the vaccine and the wild type viruses was the project main aim. 2. To assess the diagnostic value of an NS1 ELISA we first performed experimental infection trials using representative viruses of all introductions, and used the sera and recombinant NS1 antigens of the same viruses in homologous and heterologous NS1 ELISA combination. The NS1 ELISA was evidently reactive in all combinations, and did not discriminate significantly between different groups. 3. However, several major drawbacks of the NS1 ELISA were recognized: a) The evaluation of the vaccination effect in challenged birds, showed that the level of the NS1 antibodies dropped due to the vaccination-dependent virus level drop; b) the applicability of the NS1-ELISA was verified on sera of commercial flocks and found to be unusable due to physico-chemical composition of the sera and the recombinant antigen, c) commercial sera showed non-reactivity that might be caused by many factors, including vaccination, uncertainty regarding the infection time, and possibly low antigen avidity, d) NS1 elevated antibody levels for less than 2 months in SPF chicks. Due to the above mentioned reasons we do not recommend the application of the DIVA NS1 ELISA assay for monitoring and differentiation AIV H9N2 naturally-infected from vaccinated commercial birds.
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Chen, Qi, Ryan Vander Veen, Darin M. Madson, and D. L. Hank Harris. Immunization for Influenza A Virus by Intranasal Administration of Alphavirus Replicon Particles. Ames (Iowa): Iowa State University, January 2013. http://dx.doi.org/10.31274/ans_air-180814-29.

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Diaz, Leyla. Phase I Human Safety Studies of FGI-101-1A6 to Combat HINI Influenza Virus. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ada607997.

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Bosworth, Brad T., Matthew M. Erdman, Christa Irwin, Alan T. Loynachan, and D. L. Hank Harris. Evaluation of a Virus-like Replicon Particle Vaccine Expressing Proteins of Swine Influenza Virus in Pigs With and Without Maternally Derived Antibodies. Ames (Iowa): Iowa State University, January 2009. http://dx.doi.org/10.31274/ans_air-180814-644.

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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.

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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.
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Kintz, Erika, Elaine Pegg, Wendy Perry, and Wioleta Trzaska. A Qualitative Assessment of the Risk of Acquiring Avian Influenza from Poultry and Game Bird Meat Poultry products. Food Standards Agency, July 2023. http://dx.doi.org/10.46756/sci.fsa.vlf743.

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Avian influenza (AI) viruses cause infections primarily in bird species, although they are capable of spill-over infections into mammalian species, including humans. Many different strains of AI viruses are found in birds, but they can be divided into two groups based on their virulence in poultry: high pathogenicity (HPAI) and low pathogenicity (LPAI); both are capable of quickly spreading through a flock. HPAI infections often lead to severe clinical signs and high mortality while LPAI infections may not present with any clinical signs. Certain strains of AI have been associated with human case fatality rates of over 50%. Since October 2021, there has been a substantial increase in the number of AI infections reported both at commercial premises and in wild birds in the UK. The last FSA assessment on the risk to consumers of exposure to AI from the food chain was in 2015. Since the increase in infections may lead to an increased likelihood that poultry products from infected birds are entering the retail market, an updated risk assessment was commissioned to ensure advice relating to the consumption of poultry products is still appropriate. This risk assessment did not focus on the currently circulating outbreak strain but considered any AI virus. This assessment considered the risk of consumers acquiring an AI infection from poultry products, including commercial poultry, game birds, and table eggs. The risk of home processing of birds was also considered. The farm to fork risk pathway spanned from the probability that products from infected poultry would reach market to the ability of AI to cause infections in humans via the gastrointestinal route.
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Elbers, Armin R. W., Evelien A. Germeraad, José L. Gonzales, Thomas J. Hagenaars, and Clazien J. de Vos. Omgevingstransmissie van aviaire influenza virus door de lucht via wilde watervogels naar commercieel gehouden pluimvee : met een focus op transmissie vanuit HPAIV-gecontamineerde uitwerpselen van wilde watervogels via de lucht of vanuit een aerosol geproduceerd door uitademen of proesten van HPAIV-besmette wilde watervogels. Lelystad: Wageningen Bioveterinary Research, 2021. http://dx.doi.org/10.18174/556247.

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Bertke, Andrea S. Influence of Herpes Simplex Virus Latency-Associated Transcript (LAT) on the Distribution of Latently Infected Neurons. Fort Belvoir, VA: Defense Technical Information Center, February 2007. http://dx.doi.org/10.21236/ad1013850.

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